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Let’s quickly recap what we know about AD disease progression and treatments presently …

The Present: Anti-amyloid monoclonal antibody treatments

Two “disease modifying” treatments are available to patients today, and they are lecanemab (marketed as Leqembi™) and donanemab (marketed as Kisunla™). Treatments referred to as disease modifying are ones that are proven to slow the disease’s progression not just mask the symptoms as they get worse.

Two more promising disease modifying treatments are in clinical trials, and they are remternetug and trontinemab. Remternetug just complete its phase 3 trial in March as had applied for FDA approval last year, and trontinemab is about halfway through its phase 3 trial.

All four treatments focus solely on either preventing amyloid plaque from forming or aggressive plaque removal. Each may have an indirect impact on tau formation by removing amyloid protofibrils or plaque which triggers tau toxicity, but that is not their focus.

The Near Future: There is a rapidly expanding pipeline of tau‑directed treatments and combination strategies. These fall into several categories:

• Tau‑targeting therapies - The next frontier of treatments do one of three things: limit tau production altogether, attempt to prevent tau from becoming toxic, or remove tau after it becomes toxic.

• Microtubule‑Stabilizing Therapies - Since amyloid and tau both destabilize microtubules, stabilizers like lithium, may protect the shared binding site and preserve neuronal structure.

• Combination and Stage‑Specific Therapies - The future likely involves cocktail‑like treatment combinations for amyloid and tau, or stage‑specific therapy based on how far a person’s AD has progressed.

Research is increasingly showing that amyloid-beta and tau proteins are not independent villains but partners in a spiraling, destructive sequence that I call the amyloid–tau “dance of neuron death”.

• Amyloid acts upstream, becoming toxic, clumping and displacing tau from microtubules in neurons.

• Tau then becomes toxic, spreads between neurons, and causes cell death.

• If that’s not enough, toxic tau can also amplify amyloid toxicity, creating a self‑reinforcing cycle.

• Think of it this way, amyloid is the trigger, and tau is the bullet that actually kills neurons.

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Sadly, it’s not nearly that simple, there are many paths to cognitive decline in AD, and the pharmaceutical corporations may be pouring R&D into a far too narrow a treatment vector. Amyloid and tau proteins are neither the beginning nor the end of the AD progression, and that’s why we see that anti-amyloid treatments only modestly slow the disease’s progression. AD isn’t just about plaques and tangles, it’s about a brain under siege from many vectors. Each vector provides part of the story of how cognition fades and a person’s identity struggles to hold its ground.

In the scientific community, Alzheimer’s is increasingly understood as a multi‑system failure, where amyloid and tau are important but sit within a broader ecosystem of the disease. Finally, new areas are being explored more seriously…

• Neuroinflammation begins when the brain’s immune cells, meant to protect the brain, stay activated for too long. They flood the environment with inflammatory signals, damaging the very neurons they’re meant to defend.

• Vascular Dysfunction quietly starves the brain. When blood vessels stiffen or leak, oxygen and nutrients can’t reach neurons, and waste products linger. As a result, the brain’s energy, repair, and cleanup processes falter.

• Infection Connection reminds us that the brain doesn’t live in isolation. Chronic or latent infections, either viral or bacterial, may provoke immune responses that accelerate damage, turning defense into destruction. This is why scientists believe that vaccines for other illnesses like shingles, influenza, and pneumococcal are emerging as a significant way to prevent or slow the disease.

• Brain Energy Failure captures the exhaustion at the heart of the disease. Our brains use over 20% of all our energy produced, so when neurons lose their ability to utilize energy efficiently, it leaves them vulnerable to oxidative stress and unable to sustain memory and thought.

• Genetic Risk shapes vulnerability long before symptoms appear. Genes like APOE4 influence how the brain handles fats, repairs cells, and responds to inflammation, which sets the stage for resilience or risk.

• Gene Activity Changes show that Alzheimer’s isn’t just about damaged genes, but about how they’re expressed. Over time, the brain’s “software” shifts, turning protective genes down and stress genes up.

• Synaptic Loss is where the disease becomes personal. Connections between neurons, the basic component of memory and personality, begin to fray. Communication slows, then stops altogether.

• Lifestyle Factors remind us that the environment we live in and how we treat our bodies matters! Sleep, exercise, diet, pollution, and stress all shape the brain’s resilience. These are the levers we can pull without waiting for treatments to develop, it’s the place where we should all feel a sense of urgency to address in our lives. I dove deep on this in prior articles covering the “four pillars of prevention” & “what might cause AD.”

• Together, these forces converge into Cognitive Decline and Neurodegeneration, but they also point toward hope of a future where treatment means restoring balance across systems, not chasing a single vector or symptom.

This multi-pathway siege is why single‑target therapies (amyloid only, tau only) have limited impact, and why I believe multi‑modal strategies are the future.

Alzheimer’s is not a single‑pathway disease, and its treatment will not be a single‑pathway solution.

Coming Next: Our Broken Healthcare System

Peace my Friends and Thanks for Reading!

Note: What I’m sharing in my deep dive newsletter articles is based on personal research, but please remember I am not in the healthcare profession, and I have no credentials in that area past or present. I’m sharing what I’ve learned, and will continue to learn, in my own desperate effort to advocate for myself when meeting with my care team. I believe everything I share to be correct or I wouldn’t share it, but you should not take anything I say as medical advice.

I finally passed the 700-mile mark on my quest to complete all 825+ miles of the Connecticut Forest & Parks Association’s (CFPA) Blue-Blazed Hiking Trails Challenge. I’ve now completed 710 miles of the trail system and I’m locked in on earning my CFPA Hiking Challenge fleece vest for having completed it before the end of this year! The miles have been slow this winter since I had been doing my hikes by snowshoe for a few months in January, February, and March, and last fall I just wasn’t hiking while I was getting my head straight with my diagnosis. But I’m back in gear and you had better get another vest ready for me CFPA!

The CFPA is an amazing organization, they are responsible for keeping up all the state of CT’s hiking trails, as well as educating people on managing woodlands, and being more environmentally knowledgeable to protect our native wildlife and plants. CFPA is the organization I earned my Master Woodland Manager certification through in 2024, and I’m currently working on my Master Naturalist certification with them as well.

My long-awaited appointment at Mass General Brigham (MGB) Hospital’s neurology clinic finally arrived! Back in August of 2025 when I learned that the earliest I could get in to see someone was March 2026, it seemed like a literal lifetime away. Driving to Boston and back in a day was a long trip for Jan and I, but well worth the travel time. When we arrived, we checked in and were quickly brought in to collect the usual check-in information about medicines, pulse and blood pressure by an assistant, then we were brought back to the waiting room. While waiting, I thought it was odd that a doctor came out to the waiting room, found her patient and escorted them in. Then another doctor came out and did the same while greeting family members and encouraging them to come in as well. Soon after, my doctor came out, found me, introduced himself to both Jan and I, and walked us down to his office. It seems like such a small gesture, but we both loved the doctors being so patient-centric that they greet us personally and escort us in!

It only got better from there… our conversation ebbed and flowed comfortably. He would ask questions of me, I would ask questions of him, and our conversation took detours based on our replies. It was never forced, it felt like two colleagues chatting. He explained that I was assigned to him because he specializes in research and treatment of people with “early onset” Alzheimer’s (also known as young onset) and that’s how I’m categorized. That was the first of several contradictions with information my current neurologist had told me. I had asked my neurologist early on if I was considered early-onset, and he insisted that I was not early onset even though the classical demarcation is 65 years old for young versus late onset AD. I accepted it at the time because that’s what I wanted to hear, but never really believed it. So, like it or not, I fall into a class of AD patients where disease progression tends to be more aggressive.

Jan and I spent over an hour with him talking about my history, my symptoms, what Jan has observed, my test results, his approach to treatment, and the available medications and clinical trials. He got paged in the middle of our appointment and when I offered to step out so he could call in, he said “absolutely not, I’ll take this in the hallway and then we can continue.” It would have been a perfect opportunity for him to end the visit, but he didn’t end it until we were both out of questions. He reminded me of Dr Sanjay Gupta… young-ish, intensely inquisitive, and keenly in tune with cutting edge research and treatments.

All my research I’ve done on treatments was validated too. My current neurologist had shut me down abruptly when I asked about potential hybrid treatment therapies to utilize the best of the available medicines. This doctor talked about how that is becoming a best-practice for various scenarios. My current neurologist shot me down when I asked when we would be redoing the amyloid PET scan to see if the lecanemab is working, by saying it’s a waste to redo the tests. This doctor said he likes to do them at 6-month intervals when possible so that as soon as the results show a patient’s brain is “amyloid negative,” meaning the plaque levels are reduced to near zero, the treatments can stop or move to a maintenance level dose. If amyloid levels aren’t changing fast enough, then he switches the patient to another anti-amyloid treatment (lecanemab vs. donanemab). It all makes total sense, but my current neurologist made me feel stupid when asking these very questions of him.

We talked about switching over to him for all my treatment and care, but he does have one policy that would be tough. He requires patients to receive infusions in his clinic, and driving to Boston every two weeks would be an even bigger inconvenience than simply getting the infusions locally every two weeks. It would be a full day rather than 2 hours out of an afternoon. I shared how much I liked a doctor at Yale, and he selflessly raved about Yale’s memory care program, their imaging system technology, and their doctors. He asked me share all my tests with him and said he prefers to read images on his own and not rely on the tech’s reading of them. As an example, he expressed frustration that my amyloid PET scan didn’t have a centiloid measurement in it to show how much plaque accumulation my brain had. I had questioned my current neurologist on this missing data point on the PET and he told me it was a useless metric.

We agreed to take a hybrid care approach… I’d move over to Yale for my primary memory care and treatments, and I would also see him every 4 to 6 months since he specializes in my exact situation and was genuinely interested in following and guiding my progress. I hope to have “Marcus Welby” (Jan’s description of him) treating me regularly at Yale, and “Sanjay Gupta” keeping an eye me from afar at Mass General Brigham Hospital. 😋

Once I arrived at home, I set off on my next mission to make this transition happen while not missing any critical lecanemab infusions. That was going to be tricky!

First, I reached out to my insurance company, United Healthcare, to find out how to switch my primary neurologist without messing up my lecanemab infusion pre-treatment coverage authorization or missing scheduled treatments since my prior authorization was going to expire as I transitioned. I got the runaround as usual, first getting a response of “don’t worry, as soon as your new doctor requests it, you’ll be approved.” When I questioned that statement and reminded the person that it took months the last time, they asked if I could hold while they checked. 15 minutes later they acknowledged that prior authorization would take about a month. That’s a big change from instantaneous, and now puts me at risk of missing an infusion if everything doesn’t line up perfectly!

Next, I had to schedule a follow-up with my new neurologist at Yale, and of course they couldn’t fit me in until after my infusion prior authorization had already lapsed. Fortunately, they put me on the cancellations list, and within a day I had a new appointment on March 26^th! Jan and I met with him and spoke about transitioning to him for my primary memory care as the lecanemab re-authorization occurred in the next 30 days. I was surprised that he again offered to just be a second opinion and I could stay with my current neurologist. I told him that was not an option and was leaving my current neurologist regardless. He again patiently answered every question I had, and when I was heading in a direction he didn’t agree with, he had a much softer approach to sharing an alternate opinion than my current neurologist. I asked him many of the same questions I had asked the doctor at MGH and was surprised to get differing opinions on some. I shared with him that I wanted to take a hybrid approach and utilize him as my primary, while see the other neurologist at MBG as a secondary part of my care team, and he was fine with the arrangement.

I suspected I would have to change infusion centers to one affiliated with Yale, just as the doctor at MBG required if I had moved to him as primary. My new doctor confirmed that, but instead of having to drive 40 minutes to North Haven, they also partner with the infusion center at Bridgeport Hospital which is almost as convenient to get to as my current one in Stratford. I just hope the nurses are as nice as Jenn is where I go now. It’s small, she knows us all, is very friendly and proactive, and I’ve gotten to know some of the other patients there. I hear the infusion center at Bridgeport Hospital is very nice as well.

I realized afterward that having both of them as parts of my care team is ideal. “Marcus Welby” is more traditional and conservative in his approach, and “Sanjay Gupta” is more willing to embrace new approaches and treatments. With both of them having access to world-class treatment facilities and clinical trial programs, I can now feel like I’m in good hands.

Finally, I needed to speak to Eisai, the manufacturer of Lecanemab. They have a copay assistance program that helps pay for the $26K in treatment costs annually not covered by my insurance. You read that right… that’s just my insurance copay! I need to make sure that when I change doctors and infusion centers, that program doesn’t fall through the cracks. They said it was seamless, but we’ll see as I begin the transition progress. By the time I write my April update I should know how all this went and be able to share my experience with you.

Jeepers, the logistics I’ve had to navigate just to change doctors without screwing up my treatments is crazy. Our healthcare system is so BROKEN… which is an upcoming article I’m working on.

I had a former employee reach out to me this month and let me know that she has been following “I’m Still Me.” We chatted by text and decided to speak live later that week. She was part of my team in India when I worked at Dell. I had hired her and a number of others by remote interviews, and had plans to fly there for 3 weeks in February of 2020 to meet everyone and get the new team going… but COVID struck, shut down the borders, and I never got back to India in person before I left Dell in 2022. When we spoke live Lakshmi brought me to tears sharing how much the team in India appreciated my leadership, and will be forever grateful for the way I encouraged them all to learn and advance as professionals, and how I also mentored them to grow as individuals. She also shared how bad they all feel for me in terms of my Alzheimer’s diagnosis. It’s perfectly normal and compassionate to have that sense when learning gut wrenching news like this, but I assured her that I’m in a good place at this moment and no one should feel bad for me. Thank you for reaching out Lakshmi! I’m so grateful to have work friends like you. When you, your husband, and your beautiful young daughter get settled in the US this year, we’ll make plans to finally meet in person!

I got over feeling bad for myself months ago. That doesn’t mean I don’t have tough days, or tough moments, because I certainly do. Those tough times are more about my fear of the known… the more I learn about AD as I research it, the more I also learn about what lies ahead for me and my loved ones who will have to either watch it happen, or care for me as it happens. There are moments when that terrifies me. Many people with incurable diseases as afraid of dying, and rightfully so; but I’m afraid of living as a shell of my former self, and possibly being held prisoner inside my own mind as the end draws near. When I read of AD patients who periodically have moments of clarity while otherwise being unresponsive, I wonder if they are trapped within their own mind during the unresponsive times and that scares the crap out of me.

Okay enough of that, here’s some “cat therapy” compliments of Ginger & Gilligan before we transition to more good stories!

Last summer while completing the Appalachian Trail (AT) hiking through North Carolina and Georgia, I met another section hiker named Lucky Dog. He’s a “flip-flopper” meaning he started somewhere in the middle of the AT and headed south to GA, then will head south from that same spot to ME. While we were talking he said he planned to finish hiking through Maine in the summer of 2026 to complete his AT journey. I told him to let me know his plans and I’d be happy to backpack ME with him because I love the Hundred Mile Wilderness (HMW) in northern ME. Since spring is quickly approaching, I reached out to him to see what his plans are. He plans to hike ME in September, and so we agreed to meet up in Monson, ME (the start of the HMW) and backpack together from there to Mt Katahdin, which is the northern terminus of the AT. I’m so excited, I’ll get home from my backpacking trip on the Alta Via in Italy, say hello to Jan, unpack my bags, repack my bags, and head to ME to meet up with Lucky Dog a few days later to backpack one of my favorite sections of the AT!

Coming Next: Proteins Wrap-up – Summarizing amyloid, tau, their treatments, and the “next thing”

Peace my Friends and Thanks for Reading!

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Tau is a microtubule‑associated protein found primarily inside neurons in the brain. Its normal job is to stabilize microtubules, which are the internal highways that transport nutrients and signals within neurons. Tau binds and unbinds to tubules dynamically, helping microtubules grow, shrink, and adapt to the cell’s needs.

When tau is functioning normally, neurons maintain their structure and communication pathways. However, in AD, tau undergoes harmful changes:

• Tau becomes chemically modified or “phosphorylated”. Phosphorylated tau (p-tau) is tau protein that has had phosphate groups added to it. This occurrence is normal in small amounts, but in AD it becomes hyperphosphorylated.

• Once hyperphosphorylated, the modified tau detaches from microtubules, causing the microtubule network to collapse and damaging the neurons.

• Detached tau aggregates into neurofibrillary tangles, which form inside neurons.

• These tangles are toxic and strongly correlate with neurodegeneration and cognitive decline.

In fact, the number and location of tau tangles in the brain track more closely with memory loss than amyloid plaque accumulation does, but they both perform a dance together that results in the devastation we know as Alzheimer’s Disease. This relationship, or dance, is where the knowledge and research has shifted dramatically in the last few years.

Recent studies show that Amyloid can bind to microtubules with similar strength as tau, and when Amyloid accumulates inside neurons, it can displace tau from microtubules. This displacement may be the initial trigger for tau dysfunction and tangle formation.

This amyloid-tau dance unifies decades of conflicting amyloid‑centric and tau‑centric theories into a new understanding that amyloid acts upstream of tau.

Studies show that amyloid exposure accelerates tau tangle formation, and amyloid-induced synaptic dysfunction and neuron death are tau‑dependent. That means that amyloid toxicity requires tau to do the real damage of AD.

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It gets worse… clinical evidence suggests that amyloid drives tau into a toxic state, and then toxic tau can further enhance amyloid toxicity, creating a self‑reinforcing dance of death.

Some new studies also show that certain groups (e.g., Black and Hispanic adults) show higher tau levels even before amyloid buildup. This suggests that additional biological or social factors can also influence tau pathology further clarifying how complicated AD is and that its causes, progression, and biomarkers are not identical across different populations in our society.

So, you’ve now heard about three key components related to neuronal damage from Alzheimer’s disease and I’ve summarized their normal and beneficial role in the brain, their toxic role in AD, and their relationship to one another in the table below:

Scientists’ evolving understanding of the disease is reshaping therapeutic strategies too and three areas of focus have developed:

• Amyloid‑clearing therapies (e.g., lecanemab & donanemab) aim to reduce the upstream trigger.

• Tau‑targeting therapies (antisense oligonucleotides, vaccines, aggregation inhibitors) aim to block the downstream damage.

• Microtubule‑stabilizing approaches (e.g., lithium) may protect the shared binding site.

The future likely involves cocktail-like treatment combinations, or stage‑specific therapy, guided by biomarkers like Amyloid-beta42/40, p‑tau217, and tau PET.

Though I went over several anti-amyloid treatments in my prior article, the comparison below shows how the current, as well as a few emerging, anti-amyloid treatments effect tau levels in the body.

*Clinical outcome signal is the effect on composite cognitive/functional scales in early symptomatic AD

All currently approved AD treatments are amyloid‑lowering monoclonal antibodies. None of them are tau‑directed therapies, but tau biomarkers still move. When amyloid is lowered early enough and deeply enough, several trials show reduced p-tau levels in cerebrospinal fluid (CSF) & blood plasma (e.g., p‑tau181, p‑tau217), as well as slower increase in tau PET signal in early‑stage patients.

In human-speak… remove the trigger (amyloid-beta plaque), and you dampen the rate at which tau pathology spreads. Keep in mind these don’t erase existing tangles because you can’t undo existing neuronal damage.

Emerging Tau Treatment Therapies

Though tau research is significantly behind that of amyloid, there are multiple tau‑targeting therapies in clinical trials right now. They include novel approaches like monoclonal antibodies, antisense oligonucleotides, kinase inhibitors, aggregation blockers, and O‑GlcNAcase inhibitors. Several are already in Phase II and Phase II/III.

Passive Immunotherapies (Tau Monoclonal Antibodies) aim to bind to extracellular tau seeds and block neuron‑to‑neuron spread.

• BMS‑986446 (TargetTau‑1 trial) binds the microtubule binding region (MTBR), which is the core of pathogenic tau, to prevent inter-neuronal transmission of tau aggregates. MTBR‑targeting is considered more promising than earlier antibodies that failed.

• E2814 (DIAN‑TU platform trial) MTBR‑targeting antibody designed to neutralize tau seeds and is combined with lecanemab as the first major trial testing amyloid removal + tau removal together in early-onset familial (also known as autosomal‑dominant) AD.

Active Immunotherapies (Tau Vaccines) stimulate the immune system to produce anti‑tau antibodies.

• AADvac1 targets pathological tau fragments

• ACI‑35.030 targets phosphorylated tau with the goal of long‑term suppression of tau spread with fewer infusions.

Antisense Oligonucleotides (ASO) reduce tau production at the RNA level.

• MAPT‑ASO programs lower total tau in neurons. Humans tolerate partial tau reduction well, making this a viable strategy.

  Sounds scary to me to say that “Humans tolerate x well…” I’m sure someone back in the 1970s said, “Humans tolerate ingesting the chemicals that leach out of plastic well, making plastic food containers a viable strategy.”

Tau Aggregation Inhibitors aim to prevent tau from forming fibrils or break up existing aggregates.

• Small molecules that block MTBR‑mediated aggregation

• Seed‑disrupting compounds targeting early oligomers

Post‑Translational Modification Modulators - Tau becomes toxic through phosphorylation, acetylation, glycosylation, and cleavage. Several drug classes target these steps.

• O‑GlcNAcase (OGA) inhibitors increase O‑GlcNAcylation, which prevents tau phosphorylation and aggregation.

• Kinase inhibitors target kinases which are enzymes that add phosphate to another molecule and, in turn, drives tau hyperphosphorylation in the brain.

• Acetylation modulators aim to reverse tau acetylation. When proteins like Tau are chemically modified with an acetyl group, they become acetylated, are harder to clear, and begin to aggregate or clump.

Misfolded Tau Seed Blocker Therapies target tau seeds directly. Tau “seeds” are small, highly pathogenic aggregates that initiate disease spread.

• Includes DEPTAC, PhosTAC, and other chimeric molecules. Chimeric molecules are hybridized molecules that fuse parts of different molecules together. Part A performs one task and Part B performs another so they function unlike any other known molecule. It has huge promise in AD treatment where it may be able to recognize rogue proteins (part A), isolate them (part B), and remove them (part C).

Oy that’s a lot to unpack! Here’s a simpler graphic depiction I created of the investigative treatment areas… (TBT I’ve gotten pretty good at AI client prompts and many of these graphics, as well as my article cover art, are AI-generated, as is this one)

Tau‑targeting Treatment Comparison

To make all that info on clinical trials a little easier to digest for you data junkies like me, I created a comparison table. As you can see, we are likely years away from any of these making it to an FDA-approved treatment. Most are either highly specialized, or concepts that will more likely yield real human benefits a few revisions from now.

I don’t see these as something that will help someone like me with the clock already ticking, but I must admit some are very exciting! The whole field of chimeric molecules seems cutting edge but far off… chimeric compounds also occur in nature where genes have been know to accidentally fuse and viruses have been known to swap segments to form new hybrids. Chimeric molecules can occur because of mutation, recombination, or evolutionary pressure. Now scientists are using that same process to potentially cure diseases. Did you know that they’re called “chimeric” after the chimera in Greek mythology, which is a creature made of parts from 3 different animals… the head of a lion, the body of goat, and the tail of a serpent?

Does your brain hurt after reading all that? Mine sure did after researching, summarizing, simplifying, and sharing it! It felt like an endless spiral at times to convert medical gibberish into something that felt even remotely close to English. I’m sure other people have felt the same at times with my dissertations on emerging compute or communications technologies in the past!

In any case, I hope you came away feeling like you understand a bit more about amyloid and tau proteins and their relationship to Alzheimer’s disease now. I plan to release one more article on these proteins that nets it out from my perspective.

Coming Next: Month Seven Personal Update

Peace my Friends and Thanks for Reading!

Note: What I’m sharing in my deep dive newsletter articles is based on personal research, but please remember I am not in the healthcare profession, and I have no credentials in that area past or present. I’m sharing what I’ve learned, and will continue to learn, in my own desperate effort to advocate for myself when meeting with my care team. I believe everything I share to be correct or I wouldn’t share it, but you should not take anything I say as medical advice.

I want to be clear that I believe the amyloid-beta protein is a factor that causes AD to progress, I do not believe it actually causes AD. Scientists still don’t know what causes AD and that is part of what makes finding a cure so hard. Scientists have identified telltale signs like biomarkers, and physiological changes in our brains which damage neurons and cause the disease to progress, but understanding how they all fit together is still a mystery.

Let’s start with a few terms, amyloidopathy, neurodegeneration, and neuroinflammation.

Amyloidopathy refers to diseases or conditions caused by the abnormal buildup of amyloid proteins in tissues and organs. Amyloid proteins are normal in our body and they are normally soluble, but in amyloidopathy they misfold and clump together into an insoluble sticky plaque. These deposits can occur in many organs (heart, kidneys, liver, spleen, nerves), but in Alzheimer’s the brain is the primary site. This specific type of amyloid in the brain is called Amyloid-beta (Aβ) but for simplicity, I’ll just refer to it as amyloid or amyloid protein.

In AD, this buildup interferes with cell function and triggers progressive damage, also called neurodegeneration. It’s central to AD research because clearing or preventing amyloid buildup has become one of the main therapeutic strategies. Trials like the Ahead Study are testing whether monoclonal antibody drugs, like the lecanemab I’m receiving, can remove amyloid before symptoms appear, potentially preventing Alzheimer’s altogether.

There is also a growing voice in the medical community that a focus on just amyloid proteins is wrong and preventing us from getting to the heart of the solution because the amyloid research is taking funding away from trying new therapies and testing promising out of the box theories.

Neuroinflammation is the immune system’s inflammatory response within the brain and spinal cord. It is triggered by injury, infection, toxins, or autoimmune activity, and while it can be protective in the short term, chronic neuroinflammation is strongly linked to neurodegenerative diseases like Alzheimer’s, Parkinson’s, and multiple sclerosis. Chronic inflammation in general is bad within our bodies and is a focus of so many healthy living programs that include foods, exercise, and rest.

During neuroinflammation, microglia (the brain’s immune cells) and astrocytes respond to injury or infection by releasing inflammatory molecules like cytokine. These can help repair tissue but also cause neuronal damage if sustained. Normally, the blood-brain barrier (BBB) protects the brain from circulating immune cells but during neuroinflammation, the BBB can become “leaky,” allowing peripheral immune cells to enter and amplify inflammation in the brain.

Acute inflammation in the body can clear debris and promote healing, but chronic inflammation leads to oxidative stress and cell death. Similarly, in the brain chronic neuroinflammation causes progressive neurodegeneration.

There are many causes of neuroinflammation including infections, traumatic brain or spinal cord injury, autoimmune conditions like multiple sclerosis, normal aging, and environmental factors like air pollution, passive smoke, and chronic stress.

Chronic neuroinflammation is considered a core driver of Alzheimer’s progression. Sustained activation of the brain’s immune cells contributes to amyloid plaque buildup and tau tangles (which I’ll discuss in another article). Inflammation accelerates cell death, worsening memory loss and cognitive decline. That’s pretty much how Alzheimer’s Disease works.

One branch of AD research is exploring therapies that modulate inflammation, to rebalance it toward healing rather than damage and I’ll dive into some of these other research areas in future articles.

Okay, let’s dive into amyloid proteins themselves now that we have a few important terms explained.

Soluble amyloid proteins can be beneficial in their normal state. The problem arises when they misfold and aggregate into insoluble plaques. Amyloid precursor protein (APP) is a normal protein found in many tissues, especially the brain, but when APP is cut by enzymes, it produces fragments, including amyloid-beta.

In their soluble form, these fragments play helpful roles in helping neurons communicate effectively, supporting cellular repair after injury, influencing growth and plasticity in neurons, and some studies suggest it can act like part of the brain’s immune system, fighting infections.

If too many soluble amyloid fragments accumulate, they begin to misfold. Misfolded proteins clump together, forming small toxic clusters (oligomers). The clusters of oligomers eventually build up to form plaques. This plaque disrupts synapses, triggers neuroinflammation, and kills neurons. All these symptoms are hallmarks of Alzheimer’s disease.

Alzheimer’s isn’t caused by a “foreign invader” but by the brain’s own proteins turning against it when regulation fails. The real issue is imbalance: when production, clearance, or folding goes awry, the same proteins that once helped can become destructive.

I know that was a lot, so here’s a quick summary of the two types of amyloid proteins: Soluble vs. Insoluble

Soluble amyloid exists in small fragments that circulate in the brain. At normal levels, they may have beneficial roles in synaptic signaling and antimicrobial defense. When levels rise, soluble amyloid can form oligomers that are possibly more damaging to neurons than the large insoluble plaques so addressing both the plaque and the precursor may be equally important based on some theories.

Insoluble amyloid plaques are the hallmark deposits seen in Alzheimer’s brains. They disrupt brain tissue, trigger inflammation, and interfere with cell communication.

Let’s walk through the amyloid spectrum in a different way and clarify where therapies like lecanemab and donanemab intervene.

Alzheimer’s disease doesn’t begin with memory loss. It begins quietly, deep in the brain, with amyloid and tau proteins that shift from helpful to harmful. When amyloid protein misfolds and clumps, it becomes toxic, triggering inflammation, disrupting communication between neurons, and ultimately killing brain cells.

Now that you understand what amyloid protein is, let’s look at how the leading treatments address them.

Lecanemab is designed to bind to soluble protofibrils (intermediate forms between soluble oligomers and insoluble plaques). By targeting these, it reduces both soluble toxic clusters and insoluble plaque buildup. Clinical trials show it slows cognitive decline modestly in early Alzheimer’s, suggesting that removing soluble forms is beneficial because those are highly toxic to the brain.

Donanemab aggressively targets the mature plaques. It binds to deposited amyloid and helps the immune system clear them out. Clinical trials show that it too slows cognitive decline modestly and may reduce inflammation, suggesting that removing mature plaque is beneficial to preventing neuron damage.

While these treatments can’t reverse damage, both represent a shift toward disease-modifying treatments, not just symptom management.

Next, let’s bring the problem and the treatments together and walk through the stages of amyloid transformation and see where the new therapies are making their mark.

Stage 1: Healthy Amyloid

In a healthy brain, amyloid exists in soluble form. It floats freely, helping regulate synaptic activity and even defending against microbes. This is the “good” amyloid, essential, balanced, and beneficial. But when production increases or clearance falters, these soluble fragments begin to accumulate.

Stage 2: Toxic Oligomers

As soluble amyloid builds up, it starts to misfold and stick together. These small clusters, called oligomers, are highly toxic. They interfere with synaptic signaling, trigger neuroinflammation, and are believed by some scientists to be the earliest drivers of cognitive decline.

This is where lecanemab steps in. It’s designed to bind to these toxic protofibrils and help clear them from the brain before they form plaques. By targeting this early stage, lecanemab aims to slow the disease before major damage occurs. It’s also why lecanemab has both an initial clearing phase, and a maintenance phase which continues keep these toxic protofibrils in check.

Stage 3: Insoluble Plaques

Over time, oligomers aggregate into larger, insoluble plaques. These deposits clog brain tissue, disrupt neuron function, and are a hallmark of advanced AD. This where donanemab steps in, and lecanemab stays active as well.

Plaque in the brain isn’t static, its constantly shedding particles and new protofibrils are sticking to it. This is where lecanemab binds to the protofibrils on the outside and engages the brain’s immune cells to clear the plaque.

Donanemab aggressively targets amyloid plaque and clears it faster and more deeply than lecanemab as shown in clinical trials. Even after treatment ends when plaque is undetectable in PET scans, clinical trials indicate that plaque levels will remain low for another 4 years. While Lecanemab targets an early-stage form of Amyloid, Donanemab targets a later stage form that only exists in dense core plaque. This allows it to concentrate its effect on the plaque and reduce it more quickly and more deeply than lecanemab.

You may be thinking like I did, “but amyloid also has good effects on the brain, so is lecanemab doing harm by removing multiple forms of it?”

Lecanemab’s benefit is certainly for clearing soluble protofibrils and oligomers which reduces synaptic toxicity and inflammation. However, if lecanemab were to remove too much of the normal soluble amyloid involved in healthy brain signaling, that could be harmful.

Current evidence suggests the drug is selective for the toxic forms of amyloid, not the physiological baseline levels. So, the main concern isn’t loss of “good” amyloid, but rather ARIA which is swelling or microbleeds in the brain that can occur as lecanemab and donanemab crosses the BBB. This condition is closely monitored during treatment by regular MRIs which are mandated by the FDA.

It’s not inherently bad that lecanemab removes soluble amyloid. In my mind, that’s part of its strength over donanemab which focuses on removing the mature insoluble plaque form. Soluble oligomers are thought by some scientists to be the most toxic stage of amyloid driving AD progression. That’s why I chose lecanemab over donanemab given that I’m early in the disease’s progression and once the plaque is cleared, I also hope to keep the oligomers at bay as well through maintenance dosing of lecanemab.

So much is speculative at this point that I truly believe it’s a toss-up whether lecanemab, donanemab, or nothing is the best choice. I include a “nothing” choice because the benefits can be insignificantly small in some assessments of the anti-amyloid treatments.

I’m a very visual person, so here’s a simple graphic I created which summarizes all that confusing gobbledygook. It shows the range of involvement amyloid plays in AD, from the normal soluble forms that can play beneficial roles, through the toxic soluble oligomers, to the insoluble plaques. Lecanemab’s action is highlighted at the toxic stage, where it aims to reduce the most damaging forms while also lowering plaque burden. Donanemab’s action is highlighted at the plaque stage, where it aims to reduce mature plaque deposits.

Let’s wrap this long post up… Understanding the amyloid spectrum, from soluble to toxic to insoluble, helps us appreciate the amazing precision of the new therapies like lecanemab and donanemab. They’re not just clearing amyloid, they’re intervening at specific amyloid stages with specific goals:

• Lecanemab: Early intervention, targeting toxic protofibrils and indirectly on mature plaques. Think of it as targeting the smoke before a fire.

• Donanemab: Later-stage action, aggressively clearing mature plaques. Think of it as targeting the hot embers in a fire.

• If you’re like me, you’ve noticed that there would seem to be real value in extinguishing the fire, and then switching to addressing any new smoke on an ongoing basis. In other words, deploying a combination of treatments to battle AD. I’ll talk more about that in a future article.

The key for each is precision at its targeted amyloid stage, removing the harmful forms while preserving any normal benefits.

Coming Next: Tau Proteins Explained - The “other” protein in Alzheimer’s Disease

Peace my Friends and Thanks for Reading!

Note: What I’m sharing in my deep dive newsletter articles is based on personal research, but please remember I am not in the healthcare profession, and I have no credentials in that area past or present. I’m sharing what I’ve learned, and will continue to learn, in my own desperate effort to advocate for myself when meeting with my care team. I believe everything I share to be correct or I wouldn’t share it, but you should not take anything I say as medical advice.

Alzheimer’s Association - The Alzheimer’s Association leads the way to end Alzheimer’s and all other dementia by accelerating global research, driving risk reduction and early detection, and maximizing quality care and support.

Alzheimer’s Foundation of America - The mission of the Alzheimer’s Foundation of America (AFA) is to provide support, services and education to individuals, families and caregivers affected by Alzheimer’s disease and related dementias nationwide, and fund research for better treatment and a cure.

Another way to make a direct impact is to donate your time, life experiences, and genes by participating in clinical trials or studies

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Most people hear the phrase “clinical trial” and picture something unpleasant. A white‑walled lab, a clipboard, a place where other people go. People who are braver, or sicker, or more scientific than the rest of us.

The truth is clinical trials and studies are built on the involvement of ordinary people who decide that their story matters enough to share. People like us who want to help, or simply feel less alone, in the battle against AD and other diseases. Unfortunately, not enough people are stepping forward to take part.

Joining a trial or study is far more accessible than most imagine. It usually begins with a simple introspective question like I asked myself a few years ago, “Could I be part of the solution to find a cure for Alzheimer’s disease?”

From that initial question, the path unfolds gently. You search for virtual or local studies near you through a few different sites like the ALZ Prevention Registry (see my list of the top registries with links below). Once registered they send you a note when a study needs someone with your background. You don’t need to know the science behind Alzheimer’s. You don’t need to be a genius. You don’t even need to have the disease because studies and trials often look for healthy individuals too. You just need to care and be willing to help.

I used two terms a few times already… trials and studies. The difference is that in a study they are studying you, your lifestyle, your health, and your habits depending on the study. Studies also don’t involve taking any new medications or getting new treatments. Trials are for testing a new drug that isn’t on the market yet (like the promising Trontinamab drug for AD in trials right now), or testing an existing drug for treating a disease it was wasn’t originally intended for (like the recent GLP-1/Ozempik trial to see if the diabetes drug helps to prevent AD).

Every study and trial has its own rhythm. Some ask you to answer questions online every few months. Some invite you in for a memory test or a blood draw. Some explore lifestyle changes. Others test new medications. Many simply want to understand how the brain changes over time, both in people with Alzheimer’s, and in people without it.

When you find a study or trial that feels right for you, you reach out. A clinical coordinator, a real person not a chatbot, will walk you through what the study involves. They’ll tell you how long it lasts, what you’ll be asked to do. While you’re determining whether the study is a good fit for you, they’re also determining whether you’re a good fit for the study. They’ll answer every question you have, including the ones you may be embarrassed to ask.

If everything lines up, you’ll have either a virtual or in-person screening which may include a few tests or some questions. You’ll have a chance to meet the team which will walk you through the process. If the study is both right for you and you’re right for the study, you sign an informed consent form that lays out every detail before you begin. Nothing is hidden and the signing is not rushed.

Some people join trials because they want access to cutting‑edge science like me. Some because they want to help their children and grandchildren before they are affected. Some because they want to feel a sense of impact in a world of medicine that often feels like it’s cold and unapproachable.

Clinical studies and trials aren’t just research. They’re a community. They’re contribution. They’re a way of saying, “I’m still here, I still matter, and my story is part of the solution!”

Here’s how it has worked for me…

I decided 3 years ago to get help and also help others by taking a DNA test through the Alzheimer’s Prevention Registry which matches volunteers to projects and clinical trials around the country. They matched me up with an Alzheimer’s study group called Alzheimer’s Prevention Trials’ “APT Webstudy” and another called The BrainHealth® Project at the University of TX at Dallas. Part of both programs include quarterly cognitive tests which I hate because they make me face my issues. I struggle with the memory recall sections, even though I always ace the reasoning and strategy portions.

The APT Webstudy is all online. Every six months I take various tests including the Branch Test I discussed in my Sixth Week Update. It also captures how I “feel” every 3 months in terms of my state of mind… do I feel like I’ve gotten worse, am I hopeful, am I depressed, etc.

The BrainHealth Project tests are followed up by 1:1 coaching sessions to review the results and discuss how I’m feeling. I also have opportunities to join group coaching sessions with other study participants (I’ve only done that once). Last, but possibly most important, I have access to a web site and associated smartphone app to teach me techniques for living with cognitive issues and keeping my brain healthy with mental and physical exercise as well as a brain-healthy diet. Anyone diagnosed with MCI or AD, caregivers, and anyone who has family members with dementia can join the BrainHealth Project, so look into it if you’re interested in being a part of a future solution or learning how to help a loved one.

Another trial I got involved with through the registry is the Michael J. Fox Foundation for Parkinson’s Disease (PD). PD isn’t dementia, but it is another degenerative neurological disease, and it can lead to Parkinson’s-related Dementia. I’ve been reading about it and other diseases than can lead to AD, but I didn’t know that PD patients lose some or all of their ability to smell. So, when the MJF Foundation created the Parkinson’s Progression Markers Initiative (PPMI) study to test people who don’t have PD for how different smells occur to them, I decided to take part to help in the search for a cure. My grandmother had PD, and if I can help others in that area I will. The test was very easy. I was sent multiple small books of scratch-and-sniff pages that I had to scratch, smell, and select scents from a multiple-choice list that I felt most closely matched what I scratched & sniffed (e.g. pine needles, peanut butter, gasoline, etc.). The Foundation believes that this trial can lead to a better understanding of who is susceptible to the disease, and maybe longer term, what causes it. If you’re interested, you can find out more here: The Smell Test Challenge

Joining Local Trial Registries

After I was diagnosed with AD last year, my clinical study and trial priorities changed. I’m now focused on local trials that can directly help me to slow the progression of the disease. I’m still involved in the ones above, but I’m now actively seeking help as well as providing help. I signed up with registries at the two major university / medical center clinics where I’ve seen experts to help me.

Rally with Mass General Brigham Medical Center trials – I’m part of an 18-month study to track my progress with lecanemab treatments. I meet with a clinician every month for either 30 or 60 minutes of virtual cognitive tests that she administers. I also volunteered for a few other clinical trials… one which I declined to move forward with due to the excessive amount of travel required back and forth to Boston, and the other I was disqualified from due to my lecanemab infusion therapy.

Yale School of Medicine / Yale Center for Clinical Investigation – I have applied to two clinical trials at Yale for new treatments that focus on preventing or reducing Tau protein tangles in the brain. Tau is the other protein in our brain that goes rogue in AD patients and may be even more impactful than the Amyloid plaque deposits for cognitive decline. Both of those trials rejected me due to my lecanemab treatments as well. I’m seeing a trend here… sigh.

Joining National Trial Registries

While you can reach out to individual clinics like I did with Yale and MGB, the easiest way is to register with one of a few national registries which can match you with trials based on your health status, priorities and interests. Here are a few of the top ones:

Alzheimer’s Prevention Registry - Led by Banner Alzheimer’s Institute, unites leading researchers with people like you and I who are interested in taking part in Alzheimer’s studies. “We focus our work on helping scientists advance our knowledge of Alzheimer’s and its prevention.”

TrialMatch - The Alzheimer’s Association’s clinical studies matching service for people living with cognitive impairment, Alzheimer’s disease or other dementia, caregivers, and healthy participants. The database includes hundreds of studies being conducted at sites across the country and online.

The USC Epstein Family Alzheimer’s Therapeutic Research Institute (ATRI) - The USC Epstein Family ATRI coordinates worldwide recruitment of clinical trial volunteers to connect participants with trial sites.

US Dept of HHS Alzheimer’s Clinical Trials – I share this one with trepidation because I trust very little coming out of the US government right now, and even less from the moronic leaders at the Department of Health & Human Services. I know that there are thousands of good people still working hard in the organization to move critical research on AD and other diseases forward, despite the idiocy at the top, but I’d focus more on the nonprofit, politically neutral organizations first.

If you, a friend, or a loved one has Alzheimer’s, participating in a study or trial is one of the most wonderful ways you can honor them as well as helping yourself and others. Scientists can’t beat this disease on their own, they need us to work with them. Not as lab rats, but as partners in a solution for tomorrow who stand up and say, “My life and my experiences matter in the battle against Alzheimer’s Disease!”

Peace my Friends and Thanks for Reading!

I find it hard to believe that it’s been six months since I was diagnosed. In some ways it seems like just yesterday, and in others an eternity. The mental anguish of knowing what lies in my future fades with time, but any time a traumatic experience brings it back to my full consciousness, I must restart that fading process all over again. Sometimes it feels like Groundhog Day, but don’t get me started with freaking Punxsutawney Phil and his six more weeks of winter this year… I’m tired of it!

I literally just finished the longest solo road trip I’ve ever gone on, getting back on Tuesday. I drove over 2,000 miles in a six-day period for some peak-bagging I’ve been wanting to do for a year and a half. The trip planning and execution is excellent work for my brain, and the physical exertion is great for the rest of my body. TBT: after climbing three mountains in three days, I had “Frankenstein Legs,” that’s when your legs hurt too much to bend and you kind of clunk along like Frankenstein’s monster (especially going downstairs). We have had so much snow lately that 4–7-mile hikes in snowshoes just wasn’t enough to get me in shape before leaving. I drove from Connecticut to North Carolina, then to South Carolina, then to Georgia, and finally back home to Connecticut. The goal was to climb the high points in each state which are Mount Mitchell (highest peak east of the Mississippi River), Sassafras Mountain, and Brasstown Bald respectively. I’ll be writing a separate trip report about the experience for my “Where the Redfern Goes” section of my Substack so watch for the details there! The trip took a lot more planning than expected given that the region is still recovering from Hurricane Helene in October of 2024. I originally wanted to camp each night between hikes, but finding campgrounds to stay each night was very hard. So many are closed indefinitely due to storm damage, or just closed for the season since it’s still offseason for camping. Mapping out my hiking routes took some effort as well… all 3 of these mountains have roads to the top, but for me, peak bagging means climbing it on trails that were long enough to make the ascent worthwhile. I made sure all my routes were 6 to 12 miles round-trip to make me earn it!

What an awesome trip, and it was made even better by getting together with my friend John to climb Mount Mitchell in NC! I worked with John at VCE years ago, and he conveniently lives in NC. We don’t get to see each other very often, but whenever we do it is such a treat. He blew my mind one day a few years ago by just showing up on the Appalachian Trail (AT) in VA as I was backpacking through the Shenandoah Mountains. I was just hiking along solo and in a world of my own, and all of a sudden I heard someone say, “Hey Scott!” I looked up but didn’t recognize him for a second. It was one of those situations where the encounter was so unexpected that I couldn’t process it! The fact that he’s six foot seventeen (really tall) and has a British accent should have clued me in, but I just wasn’t expecting to see someone I knew on the trail that day! We’ve also had fun peak-bagging in NH several times including awesome winter ascents of Mt Washington and a brutally cold hike up Carter Dome. Thanks for joining me John! It’s so much more fun hiking with someone when I have the opportunity.

I love Valentine’s Day! Not for the gift-giving though. Every year I make Jan a special dinner. I spend a few weeks researching new recipes that I can make with red foods or that I can color red with natural juices like beet and pomegranate. This also happens to be one of the beneficial brain exercises I discussed in “Four Pillars – Part 3” of trying out new recipes! For our dinner, I made Spaghetti Al Assasani, heart-shaped biscuits from scratch, heart-shaped beets marinated in red wine vinegar & spices, heart-shaped Jello gelatin-pudding cutouts, and Valentine heart blondies. The spaghetti caught my eye because I love to make risotto from scratch and this variant is made in a similar way with a spicy tomato broth I made from our bumper crop of tomatoes from our garden last summer. The raw spaghetti is laid in a deep sauté pan with the first cup of broth and allowed to char on one side as the broth cooks down and absorbed to give it flavor. After that the broth is added gradually allowing the spaghetti to absorb it until you have a wonderfully broth-infused pasta dish! I used my many different sized heart-shaped cookie cutters to shape the hand-rolled biscuit dough, beets, and Jello (pudding/gelatin) treats. I cut out a heart-shaped center in each of the blondies and filled them with frosting made from scratch that was colored pink from pomegranate juice that added a tangy citrus flavor to soften the sweetness from the frosting and blondie. As always, I add some cut flowers to the table and found a romantic playlist for background music (Spotify makes that easier nowadays rather than curating one myself like I used to). Lots of work but lots of fun too! Jan deserves it, she is an amazing partner and my best friend who indulges in so much of my nuttiness! I love you so much Jan!

Because I decided to go public with my AD diagnosis, I know that I’m periodically going to be stereotyped by people. I also know that it will usually be unintentional and well-meaning, so I’m going to do my best to handle it with grace when it occurs. Jan and I went on an outing with a group recently, and I decided to go out on my own for a bit because no one else wanted to tackle an activity as challenging as I wanted to. I let Jan know where I was going, when I’d be back, and I had my Garmin inReach Messenger emergency beacon with me as well. While I was out a few people mentioned to Jan their surprise with my diagnosis, and separately, their concern for me doing such a long and hard activity (it wasn’t hard or long for me at all). They ended up sending a person out to check on me. We crossed paths when I was almost back and we laughed about him being sent out for me, he decided to continue on to get some added exercise as well, and I let him know that I’d inform everyone that we had crossed paths. When I got back it seemed like everyone heard about me going out, and I tongue-in-cheek let people know I had crossed paths with Joe and I assured them he was safe and doing fine. 😊 I know people who don’t know me will wonder at times if I should still be challenging myself in the same ways I always have, and they also don’t realize that what is a hard or long activity to others is a short, fun outing for me. I am committed to gracefully understanding when people worry, but also persisting in challenging myself at every opportunity. I have always said that when I die, I want to go on a mountain top somewhere, but that time isn’t here yet!

My friend Scott whom I worked with years ago at EMC reached out to me after my AD announcement and let me know he and some friends are going on a trip to Italy this year to hike the Alta Via 2 (AV2) route through the Dolomite mountains and he asked if I’d be interested in coming as well. Once I talked to Jan (who said, “do it!”) I accepted and I’m SO excited! There are 6 AV routes through the Dolomite Mountains, and each one has sections where hikers must traverse “via ferrata” which is Italian for “iron way” because those sections require you to traverse rugged ledges, slopes, and cliffs on iron rungs or holding onto braided steel cables while clipped in with a harness. The higher the route number the more complex the routes are, so AV2 isn’t terrifyingly challenging, but it’s absolutely gorgeous scenery and the via ferrata sections will be fun. I don’t like heights, so these types of activities are always fun to confront that anxiety … TBT despite not liking heights, I’ve jumped out of two perfectly good airplanes, crossed crevasses in glaciers on ladders, and gone up in a hot air balloon, so this isn’t a stretch for me at all. Thank you Scott for recognizing that “I’m still me,” and inviting me on the trip despite my diagnosis!

Finally, I’m SO excited! After months of waiting, Jan and I are finally meeting with the specialists from Massachusetts General Brigham Medical Center’s memory care clinic next week! While we’re up in the Boston area, we are going to visit with some friends we haven’t seen in too long. I’ll share the results of that clinical evaluation in next month’s update, I have lots of questions for them. While I look forward to another expert opinion, I dread the inevitable hours of cognitive tests they’ll put me through.

Now that we’re all caught up to the present, the frequency of my articles will slow down. I’ll release one article each week or so with a monthly personal update. Writing has felt like a full-time job to get you all caught up, and I want to get back to releasing more articles for my other newsletters within “Trails, Truths and Thoughts” for Where the Redfern Goes, Freedom Ink, and Clearing the Air. I’m also still aspiring to do some audio & video podcasts but that hasn’t been possible to develop with the torrid pace of my initial I’m Still Me writing.

Coming Next: Clinical Studies & Trials – Essential tools and not just for sick people

Peace my Friends and Thanks for Reading!

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It’s February 6, 2026, and I’m still me. 😊 It’s now been over 5 months since my diagnosis. I think I should have stayed with bi-weekly updates because SO much newsworthy occurred this month… both good and not so good, but not bad. This is a long post, but there is a lot that I feel is important to share so please indulge me. ❤️

I had two MRIs since my last update, my 2^nd & 3^rd of the treatment schedule. Both were free of ARIA once again and I’m still happily “Unremarkable” LOL! I have one more MRI at the 6 month point and at that point the risk of ARIA will be generally behind me. I’ve been fortunate with absolutely no side effects from the infusions, and hopefully they are doing their job inside my brain by clearing the plaque.

Some things I do while researching my disease for upcoming articles are not helpful for my emotional wellbeing. I was investigating some statistics for my articles on the impacts of federal healthcare budget cuts (upcoming) and the devastating effects of budget cuts on AD research, and I got into researching the life expectancy of a person diagnosed with Alzheimer’s Disease (AD). An organization called Dementia Care Central has an Alzheimer’s life expectancy calculator based on your specific information. If you enter your age and answer a few questions about your disease progression and other demographics, it’ll estimate how much longer you’ll live independently, and how long before you’ll die. I knew better, but I entered my information! Even though I feel great, statistics don’t lie and I can’t hold this disease off forever. Here’s what it returned for me:

“It is expected that the individual will require a nursing home level of care between 4 yrs & 4 mo and 6 yrs & 7 mos from today.” To be clear, this does not mean they will need to enter a nursing home. Many individuals receive nursing home level of care outside of nursing homes. “Nursing home level of care” is a formal designation as to the types and amount of care an individual requires.

It went on, “It is expected that the individual will pass away between 5 years, and 7 years and 6 months from today.” This is an estimate based on the outcomes of persons with similar demographics and similar symptoms. This information is provided to better allow families to plan for their futures.

If you have AD, DO NOT run your own information through this calculator! Trust me, nothing good can come from it! Instead of enjoying my day, I was running scenarios through my brain trying to justify why I will be different, and how their data is based on patients who did not have access monoclonal antibody treatments like Lecanemab that I’m already on. This really rocked my world again… I guess I was hoping to see something like 15-20 years to make me feel better, but it backfired. 🤷‍♂️

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January was the month that I launched my “I’m Still Me” newsletter that you’re reading now. Thank you for coming to Substack and sticking with me! I had delayed the planned launch several times from November through the holidays, so my news didn’t overshadow them for our family… and I guess I just wasn’t emotionally ready to go public either. The response has been surprising from you all. Plenty of people have offered their encouragement, sympathy or shock which is appreciated. For all you who are still reading these updates a few months in, that wasn’t my desired result. What will define my success is if my journey, hard as it is for me and my loved ones, when shared with people, helps them to understand Alzheimer’s better or motivates them to see a neurologist to get in front of symptoms they are experiencing themselves, or encourages them to speak to a loved one about doing the same.

Sharing my story with the world has also resulted in many people reaching out to me. I’ve been approached by an organization named “Being Patient” about doing a short video interview with them about my journey to my diagnosis and life since “D-Day”. When I do it and it’s published, I’ll share it in “I’m Still Me” as well since I’d like to do more video & audio posts as podcasts in the future. Other individuals have also reached out to me including a man who is telling the story of his time as a caregiver for his sister who had multiple forms of early onset dementia. His story is called “Five and a Half Years”. The title heartbreakingly corresponds to the length of time between his sister’s diagnosis and her passing. Others have shared their concerns and learnings on their own journeys.

I don’t seek attention for me, because that’s actually proving to be a detriment. An unintended consequence of all this attention is being forced to face my own mortality once again. I had packaged that away a few months ago and was living a blissfully ignorant life again. Now as I reread and edit those dark initial months, research even more for new articles, and talk to people in different phases of their own AD journeys I’m reminded of my journey with a demon that won’t relent. I appreciate all the people who keep saying, “you’re strong, you can do this,” but the reality is that I can fight my best fight, but medical science to-date says it’s a fight I can’t win. I see that even more as I speak to other fighters who were living a great life but just ended up being a punching bag for this f*cking disease in the end.

Yeesh! Now I’m back in that dark place that I thought I had left behind a few months ago questioning every little thing I forget, torturing myself over every little speech disfluency, and struggling to sleep at night. It’s got me thinking that maybe I’m already slipping and I just don’t realize it… you know, like the story of the lobster in a pot of slowly boiling water who doesn’t realize what’s happening until it’s too late.

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On the more positive side… even though I was disqualified from one of the clinical trials I had volunteered for, the program shared the information with me on their over-the-counter supplement in case I wanted to take it on my own. I inelligible because I’m receiving lecanemab infusions which could have positive benefits of its own and makes it hard for the study to know what cognitive benefit came from lecanemab versus the supplement. The supplement is one of the ones I discussed in the “Four Pillars – Part 1” called nicotinamide riboside (NR). So, I’m beginning a regimen of 500mg of NR daily now that my PCP approved it, and will increase to 1,000mg over time, which is what the study is using. They say it takes 3 weeks to feel the positive effects, so we’ll see if it improves my clarity and those annoying little speech disfluencies!

Speaking of clarity… I feel like I’m the most tested person in the world on cognition. Every time I visit a neurologist, they administer a MoCA test to me. Every six months I have to take a 5-day BRANCH test for the Alzheimer’s Prevention Trial (APT) WebStudy and every 3 months I have to answer questions on how I’m feeling in terms of my memory, social interactions, ability to perform daily tasks, etc. My BrainHealth Project clinical study also requires me to do quarterly online testing and then have a counseling session to talk about the results. Finally, every month I’m tested live by Zoom with a clinician for the REAL Outcomes program at Mass General & Brigham Hospital to track my cognition with respect to my lecanemab treatments. This month ALL of them except the BRANCH test coalesced in a 1-week time period… oof!

I had been dreading my tests this month because I could feel that I didn’t do well on my REAL Outcomes test last month, and a downward trend would be bad … especially for my emotional stability right now. Thankfully I breezed through the REAL Outcomes test without any issues even when I was stiff-arming my cat Gilligan because he had jumped up on my desk and wanted to join the meeting right in the middle of a “speed of processing” test where I was calling out what I was seeing on my screen as they rapidly flashed by! When that segment ended, I asked my clinician Sarah how I did and she said it went flawlessly. She asked if I was dealing with a cat because she could see my arm extend straight out to the side mid-test... and right on queue Gilligan walked in front of the camera blocking her view of me! LOL

I also had to take my quarterly cognitive tests for the BrainHealth Project (online and automated) and the APT WebStudy (also online and automated). I felt like I rocked them both! Then I had my quarterly follow up with my neurologist whose assistant administered yet another MoCA test and I aced that too, even the memory portion of the test. So, in a 1-week period I had 4 different cognitive tests that each lasted from 15 to 90-minutes and I was on fire in every one of them. That is a load off my mind.

It’s humorous in a warped way looking back at the week because I was very anxious about each test and lost considerable sleep worrying about them… what if they show I’ve gotten worse and the disease has progressed? As I’ve said before, the mind games I’m experiencing since being diagnosed are far more debilitating presently than the disease itself.

The 3-month follow-up with my neurologist came with conflict yet again. I rocked my MoCA test with his assistant which had me feeling good, until he walked in. I told him I plan to go to Antarctica next January and the expedition organizer might ask for a doctor’s note of confidence that I can handle the trip given my AD diagnosis (yes, I was honest on all my medical paperwork). I asked him what he thought about me going, and his answer was, “The glaciers are melting.” Correct observation of the devastating impact of climate change and a slightly amusing quip, but not what I was asking. So, I asked more directly if he would be willing to provide a recommendation if needed. He proceeded to educate me on cold weather safety to which I thanked him and assured him I’m an expert in winter mountaineering, all I need is his approval that I’m cognitively fit. He then started debating with me that I’m so early in the disease progression that there is no need for that. I told him I wasn’t the person who needed to be convinced, it’s the expedition organizer. So, I asked again if he would provide a letter if needed and he went back into why it was overkill because I have no symptoms. I had to cut him off and ask yet again, “will you or won’t you provide a letter stating that?” He finally agreed.

Everything is a fight with this guy… Later he asked me how I was feeling now that I’m taking the Aricept (donepezil) he prescribed. I told him that I decided not to begin taking it. I feel generally fine, aside from the minor speech disfluency issues that other people don’t even notice. As a result, I see no compelling reason to start taking a drug that has many potential side-effects and does nothing to slow the disease. He got visibly annoyed and started arguing with me. He told me the donepezil would cure the speech disfluencies. I asked him point blank if that was a fact or an assumption, to which he backed off and said, “well, it might help.”

I am so done with his bullshit, he acts like a petulant child whenever I don’t blindly accept what he says without question. It’s MY life dammit, and I’m gon’na keep advocating for myself and asking questions of him, or someone else better in the future!

For hanging with me on this month’s update, you deserve a double dose of cat therapy! So, here are a few more pics of our cat, Gilligan…

Coming Next: Finally Catching you up to date with my Six Month Update for February!

Peace my Friends and Thanks for Reading!

Alzheimer’s risk isn’t only about genes, it’s also about epigenetics. In human-speak, it’s about how your lifestyle choices can influence how your genes behave. In this case, healthy habits can lower your chances of developing Alzheimer’s disease (AD).

That’s right… your living habits can help you PREVENT Alzheimer’s Disease! Forget about those ads for miracle supplements, they don’t exist. You are your own best weapon, or your own best enemy, in the battle against AD.

Subscribe now

Numerous studies show the relationship between lifestyle choices and AD. The FINGER study in Finland of ~1,200 people over two years proved that a mix of healthy diet, regular exercise, social activities, and mental challenges can greatly reduce AD risk in people already vulnerable. Additionally, the MAPT study in France found similar results, showing that lifestyle changes across multiple areas can cut risk factors.

These findings match the “four pillars” approach promoted by groups like the Alzheimer’s Research & Prevention Foundation and the Alzheimer’s Association which found that the secret to prevention is connections. Brain connections (keeping your brain cells active and healthy), social connections (staying engaged with other people), lifestyle connections (eating well, exercising, and stimulating your mind), and emotional connections (maintaining psychological well‑being and balance).

Healthy daily choices like good food, movement, socializing, and mental activity can protect your brain and even slow decline. There’s no cure yet for AD, so prevention is about staying connected to your body, your mind, and the people around you. Even small changes in daily habits can make a big difference.

If you stuck with me for the articles on all four pillars including diet, stress management, fitness, and spiritual wellbeing then your head is now swimming with new ways to strengthen your brain health. The bad news is that you have TONS of new ways to do it and your probably overwhelmed on where to start. Don’t despair, I was prepared for that!

Here’s a sample weekly brain‑healthy routine I put together that blends mental challenge, physical activity, social engagement, and restorative habits. It mirrors the combination that research consistently shows is most protective against age‑related decline.

It’s structured, doable, and flexible enough for real life whether your still working, retired and “busier” than ever (like me), or retired and kicking back for a while.

The strongest cognitive protection comes from mixing mentally challenging games & tasks, physical activity, social engagement, GOOD sleep (not just adequate), and stress reduction together into your daily routine… EVERY day.

Weekly Brain‑Health Routine

Daily Foundations: These are the “non‑negotiables” that you must do to keep your brain healthy.

20–30 minutes of brisk movement: Walking, cycling, dancing, or anything that elevates your heart rate. Aerobic activity increases blood flow, supports neuroplasticity, and boosts BDNF (Brain Derived Neurotropic Factor – a protein that helps neurons grow, survive, and communicate).

10 minutes of mental training: Rotate between these categories (see “Pillar 3” article for details on these exercises):

· Memory (recall lists, names, details)

· Executive function (logic puzzles, strategy games)

· Language (word generation, reading aloud, learning a language)

· Speed‑of‑processing (visual search, fast matching tasks)

5–15 minutes of mindfulness or breathwork: Reduces stress hormones that impair memory and attention. (see “Pillar 2” article for details on these)

Social contact: A conversation, a shared activity, or even a phone call.
Don’t forget that lack of social engagement is one of the strongest predictors of cognitive decline, but activity builds resilience!

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If you want to break it all down into a weekly structure, here’s a daily approach. You can also mix and match within each day, the permutations are limitless!

Monday - Memory & Planning

• Memory exercise: recall a list of 10 items after 30 minutes

• Plan your week out on paper. It engages executive networks in your brain

• Go on a 30‑minute walk outdoors

• Read for 20 minutes in the evening and summarize the main points

Tuesday - Language & Learning

• Learn 5–10 new words in a foreign language

• Write a short paragraph summarizing an article you read, and share it with someone

• Call a friend or join a group chat

• Perform strength training or yoga

Wednesday - Executive Function Challenge

• Strategy game: chess, sudoku variant, or a logic puzzle

• Try a “Stroop‑style” task (see “Pillar 3” article for details and the MindCrowd Project web site)

• Explore a new walking route at a park

• Relax and destress from the day with a mindfulness session before bed (Pillar 2)

Thursday - Creativity & Novelty

• Try a new recipe, hobby, or craft

• Listen to music from a new genre

• Perform 20–30 minutes of aerobic exercise

• Write down three things you learned today

Friday - Spatial & Navigation Training

• Draw a map from memory (your neighborhood, a recent trip)

• Do a jigsaw puzzle or mental rotation task (Pillar 3)

• Take a walk without GPS and navigate intentionally

• Go on a social outing with friends

Saturday - Deep Learning Day

• Longer cognitive session (30–45 minutes) in any category

• Read a chapter of a book and discuss it with someone

• Outdoor activity for at least 45 minutes

• Light reflection journaling

Sunday - Recovery & Integration

• Gentle movement: stretching, yoga, or a casual walk

• Review the week: what felt mentally stimulating?

• Prepare one new challenge for the coming week

• Early bedtime to reinforce memory consolidation

Optional Add‑Ons: Whenever you are inspired…

• Practice Music: Playing an instrument or singing (you don’t want to be around me if I do this!)

• Art or photography session

• Volunteering or community engagement

• Brain‑healthy cooking day (Pillar 1 - omega‑3 rich meals, colorful fresh fruits & veggies, high fiber options)

Coming Next: My 4 month update - January

Peace my Friends and Thanks for Reading!

That’s right… your living habits can help you PREVENT Alzheimer’s Disease! Forget about those ads for miracle supplements, they don’t exist. You are your own best weapon, or your own best enemy, in the battle against AD.

Numerous studies show the relationship between lifestyle choices and AD. The FINGER study in Finland of ~1,200 people over two years proved that a mix of healthy diet, regular exercise, social activities, and mental challenges can greatly reduce AD risk in people already vulnerable. Additionally, the MAPT study in France found similar results, showing that lifestyle changes across multiple areas can cut risk factors.

These findings match the “four pillars” approach promoted by groups like the Alzheimer’s Research & Prevention Foundation and the Alzheimer’s Association which found that the secret to prevention is connections. Brain connections (keeping your brain cells active and healthy), social connections (staying engaged with other people), lifestyle connections (eating well, exercising, and stimulating your mind), and emotional connections (maintaining psychological well‑being and balance).

Healthy daily choices like good food, movement, socializing, and mental activity can protect your brain and even slow decline. There’s no cure yet for AD, so prevention is about staying connected to your body, your mind, and the people around you. Even small changes in daily habits can make a big difference.

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Pillar 4: Spiritual Fitness

When I use the term spiritual, it’s not related to religion, it’s a broader practice of tuning into what feels most deeply true, meaningful, and connective in your life. In other words, the experiences, values, and relationships that expand your sense of self and anchor you in something larger than your day‑to‑day concerns.

Meditation is more than just a way to relax and relieve stress, it strengthens psychological well‑being by helping you accept yourself and others, boosting confidence, reducing negative thoughts, and creating a foundation for personal growth and meaningful living. Taking that a step further… when you feel connected to others, serve your community, and live with purpose, you not only gain greater fulfillment but you also lower your risk of memory decline.

Practices that cultivate gratitude, strengthen community ties, and reinforce meaning don’t just “feel good.” They focus your attention, regulate stress, and support the networks in the brain that handle memory, emotional balance, and resilience.

Still not quite sure how to build your spirituality through actions? Here are some simple activities that anyone can do that reliably strengthen those three pillars of spirituality: gratitude, connection, and meaning.

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Reflective moments that build Gratitude

Daily “Three Moments”

Write down three specific things that went well today and why they happened. The “why” is what trains the brain to notice causes, not just outcomes.

Savoring Ritual

Pick one ordinary moment each day: your first sip of tea or coffee, sunlight bathing a wall of your home, a warm conversation with a friend, your daily cuddle with your pet, crickets chirping at sunset. Spend a minute deliberately experiencing it. This strengthens your brain’s reward and attention circuits.

Gratitude Letter (Sending it is optional)

Write a short letter to someone who shaped your life. Reading it aloud to yourself activates emotional processing and memory networks. I’ve done this from time to time and have actually sent them to the people. It makes me feel good and I hope it feels equally rewarding for the people I reach out to. You’ll notice that I add slightly vague notes of gratitude in my personal AD journey reflections I posts that hopefully are seen by the person I intend them for.

Gratitude Walk

Take a 15-minute walk and name things you appreciate in your environment: colors, sounds, people, smells, memories. This blends movement, mindfulness, and positive attention which is a powerful combination for brain health. I am regularly doing this on my hikes. Even on the hardest days that I would categorize as miserable, I take time to slow down and acknowledge what I’m most grateful for in my surroundings and it makes the day instantly better!

Community Activities That Build Connection

Weekly “Anchor Conversation”

Choose one person you talk to every week, a friend, sibling, or neighbor, and make that your anchor conversation to maintain. The consistency matters more than the length.

Join a Purpose‑Aligned Group

Book club, advocacy group, faith community, volunteer team, hiking group. Anything where people gather around shared values. Regular group belonging is one of the strongest predictors of cognitive resilience. This is what I love about my CFPA Master Naturalist course and work on the Appalachian Mountain Club’s Conservation Committee. We are kindred souls trying to save our planet. In a world that seems so self-centered, it’s nice to spend time with people who want to save something.

Skill‑Sharing Exchange

Offer something you’re good at to a person you know (cooking, writing, tech help) and ask them to teach you something. Reciprocity strengthens social bonds and stimulates learning networks.

Micro‑Acts of Community

Comment thoughtfully on someone’s social media post and build on their idea rather than tearing it down. Bring a neighbor’s garbage bin up to their door. Share an article with a personal note. These tiny gestures reinforce your identity as someone connected to others.

Activities that reinforce purpose and direction to build Meaning

Weekly “Why I Do This” Reflection

Pick one part of your life: work, caregiving, advocacy, creativity. Write a few sentences about why it matters to you. This stabilizes your sense of direction & purpose and reduces stress.

Values Check‑In

Choose one core value (kindness, justice, curiosity, courage) and ask yourself, “What did I do this week that aligned with this value?” This keeps your actions tethered to meaning.

Legacy Moments

Record a short voice memo about a lesson you’ve learned, a story from your life, or something you want future generations to know. This strengthens autobiographical memory and reinforces identity. I’m beginning to do this now to preserve some of my most cherished moments and learnings before they are gone.

Purposeful Micro‑Goals

Set one small, meaningful goal each week that’s identity‑based , not productivity‑based.
Examples:

• Reach out to someone who might feel alone

• Learn one new thing about Alzheimer’s science, climate change, etc.

• Do something that reflects the type of person I want to be remembered as

Now, put it all together in a simple weekly rhythm for you and your brain. Break it up into different days so it doesn’t feel overwhelming… this needs to build inner peace, not create stress. Here’s a sample:

Monday — Gratitude walk
Tuesday — Anchor conversation
Wednesday — Values check‑in
Thursday — Skill‑sharing or community activity
Friday — Meaning reflection
Saturday — Gratitude letter or legacy memo
Sunday — Quiet savoring ritual

Researchers agree that having a clear sense of purpose in life is linked to better health outcomes across the board. People who believe their lives have meaning show stronger resilience against AD, as well as other conditions like stroke and heart problems. Positive emotions such as love, compassion, and gratitude also protect the brain by calming the body’s response to stress and supporting long‑term brain health.

Recent research shows that spiritual well‑being may help preserve brain regions tied to memory and attention in people at risk for AD. Studies even suggest that it may slow the progression of AD.

Practicing meditation, cultivating positive emotions, staying socially connected, and living with purpose are powerful ways to protect your brain and overall health. These habits are easy to begin. Set aside time each day to reflect, focus on gratitude, engage with supportive communities, and remind yourself of the meaning in your life. Over time, these practices can help you age with resilience, clarity, and purpose.

Coming Next: Four Pillars of Alzheimer’s Disease Prevention – Wrap Up

Peace my Friends and Thanks for Reading!

That’s right… your living habits can help you PREVENT Alzheimer’s Disease! Forget about those ads for miracle supplements, they don’t exist. You are your own best weapon, or your own best enemy, in the battle against AD.

Numerous studies show the relationship between lifestyle choices and AD. The FINGER study in Finland of ~1,200 people over two years proved that a mix of healthy diet, regular exercise, social activities, and mental challenges can greatly reduce AD risk in people already vulnerable. Additionally, the MAPT study in France found similar results, showing that lifestyle changes across multiple areas can cut risk factors.

These findings match the “four pillars” approach promoted by groups like the Alzheimer’s Research & Prevention Foundation and the Alzheimer’s Association which found that the secret to prevention is connections. Brain connections (keeping your brain cells active and healthy), social connections (staying engaged with other people), lifestyle connections (eating well, exercising, and stimulating your mind), and emotional connections (maintaining psychological well‑being and balance).

Healthy daily choices like good food, movement, socializing, and mental activity can protect your brain and even slow decline. There’s no cure yet for AD, so prevention is about staying connected to your body, your mind, and the people around you. Even small changes in daily habits can make a big difference.

Pillar 3: Exercise

Both physical and mental exercise are essential for keeping the brain healthy and lowering the risk of Alzheimer’s disease. Physical activity increases blood flow to the brain, boosts important compounds like BDNF (brain-derived neurotrophic factor), and even stimulates the growth of new brain cells. Research at Columbia University showed that older men who exercised on a treadmill for just thirty minutes, four times a week, grew new cells in a part of the brain linked to memory and thinking. The encouraging news is that these benefits can be experienced at any age, regardless of fitness level or cognitive decline.

Experts recommend about 150 minutes of aerobic exercise each week, along with a few sessions of strength training. But even mild activity makes a difference. Something as simple as a brisk 20–minute walk three times a week can improve memory and focus. For those already in good shape, adding variety and intensity to their weekly routine such as hiking (my favorite), swimming, tennis, cycling, or group classes, can provide even greater benefits. The most important thing is to choose activities you enjoy and make them a regular part of your routine. If you can find a friend that you enjoy spending time with and exercising with, who will push you beyond your usual comfort zone, that’s even better!

We all know ways to get in our physical exercise, we just may not do enough of it, so I’m going to spend more time here talking about the underestimated but crucial form of exercise … mental exercise! Alzheimer’s prevention isn’t only about physical fitness, it’s equally about staying mentally challenged through learning and conditioning. Combining both creates the strongest protection for long-term brain health.

Just as the body needs exercise, the mind does too. Keeping the brain active helps prevent decline and strengthens cognitive abilities. Reading is one of the best ways to stay sharp because it forces the mind to learn and think beyond everyday tasks. Other activities like listening to, or playing, music, creating or viewing art, playing games that require thought, and solving puzzles also challenge the brain and give it a healthy workout.

Here are some routines and activities to exercise your brain in six different ways:

Memory‑Training Tasks

Repeated retrieval practice is one of the strongest ways to reinforce neural pathways. These exercises strengthen the hippocampus and frontal networks involved in recall and attention.

• Learning new names and trying to recall them later. I do this to try and burn them into my memory, so I remember when I see them again

• Memorizing short lists, then increasing difficulty ¹ Another one of my monthly cognitive tests that I don’t love

• Practicing “dual encoding” (pairing a name with a visual image to learn and remember) There’s a cognitive test I take quarterly and I have to associate names with faces, so I try to associate the name, face, and a reason in my head (e.g. Rita has red hair, John looks like my friend John)

Executive Function Challenges

Executive function is a major predictor of long‑term independence, so keep planning and problem solving! Without exercise, these areas often decline early.

• Strategy games (chess, bridge, Go, sudoku variants)

• Switching tasks with rules (e.g., “say the color, not the word” like Stroop tasks) ¹ This is part of my monthly cognitive tests, I first have to call out the colors left to right and top down in a matrix of dots, then I have to read the words of colors printed in black and white in a similar matrix, THEN they have names of colors that are not color-coded (the word “red” is printed in blue ink) and I have to call out each based on the color its printed in, not the word itself. Oh yea, and I have to do it as fast as I can!

• Timed problem‑solving challenges ² I love problem solving so this is fun for me and I look for opportunities to troubleshoot something on my own. Who needs a manual?!

Language‑Based Exercises

Language networks in the brain are sizeable and respond well to training, and related tasks involve multiple brain regions simultaneously.

• Learn a new language. I’m going to have to learn a little Portuguese and Italian before a few trips this year!

• Read aloud ¹ A part of my monthly tests to check reading fluency & expression

• Write summaries of articles or books ^1,2 I’m doing a whole lot of this by reading articles on AD and summarizing what I learn for you all. It’s also part of my monthly testing that is sometimes paired with reading aloud.

• Word‑generation tasks (e.g., list as many names of animals starting with “B” in 60 seconds) ¹ Yup, another part of my monthly testing. The funny thing is I often freeze up on this easy one… I guess it’s the pressure? 🤷‍♂️

Spatial and Navigation Training

Spatial memory is closely tied to early Alzheimer’s changes. Strengthening spatial networks in the brain may help compensate for early declines in the hippocampal region of the brain.

• Mental rotation puzzles (e.g. rotating an object in your mind to visualize what it looks like from other angles)

• Investigate then navigate a new route without using your GPS ² I’m doing this multiple times a week as I plan out new routes to hike, and complex optimizations to cover as many trails as possible, in the shortest distance possible when they criss-cross.

• Drawing maps from memory ² I look at a map, and then recreate it in my mapping app called GaiaGPS to take with me on the trails. Though I usually complete my hike from memory and not open my app.

• Jigsaw puzzles ² Jan and I have been doing many more of these lately. I like to put sections together without looking at the picture and simply looking for shape and color patterns to assemble it.

Speed‑of‑Processing Exercises

Fast processing games support better memory and executive function as well as helping to maintain reaction time and attention.

• Computerized training that flashes stimuli quickly ^1,2 I enjoy this type of game/training, but it’s also part of my monthly testing.

• “Where’s Waldo” types of visual search tasks

• Fast‑paced matching games ¹ Yup, another part if my monthly testing… but I enjoy these parts. It’s the memory parts I dislike.

  ---

Creativity and Novelty

Stepping out of your comfort zone to learn something or have new experiences triggers a dopamine release in your brain, which makes you happy, and enhances learning & memory.

• Learn to play a musical instrument or paint. I still keep saying I’m going to learn to play the harmonica…maybe one day… ²

• Take up photography or crafting

• Trying new recipes or hobbies. I love to cook and try out new recipes, and Jan loves to enjoy them with me! ²

• Exploring new places. Get out and travel or just visit new parks in your area to go for a walk. (this can also exercise your navigational skills too!) ²

• Take a class at the local community college or get certified in something you’ve always wanted to know more about. I’m on my fourth conservation certification in the last 3 years. ²

This all may seem overwhelming, but you don’t have to search for where to find. The items with a superscript “2” above I’ve shared how I use or play them to help you visualize doing them as well. The items with a superscript “1” are games, activities, & exercises that can be played at the links below:

• The MindCrowd Project, which I had mentioned in one of my earlier articles, has many different brain exercises.

• BrainHQ is a for-profit brain training site, but there are a few free exercises you can use. Most require a subscription, but they are challenging and entertaining.

• If you’re old-ish like me and a member of the AARP, the AARP.org web site has both free access and members only games to play.

• My family loves to play the games on puzzlist.com and share our results with each other. It’s hard competing with librarians and reading fiends but I do my best! 🤣

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If you know me, you’ll know that my favorite activity is hiking in the backcountry, which requires both physical and mental exercise. The physical part is obvious, but mental components occur both before and during the activity. Beforehand I’m planning and optimizing routes on interconnecting trail systems, during my hike I’m following that route from memory and working out challenges with map orientation & reading, weather prediction, safety issues, and regularly determining my current location.

Find the exercises that excite you, it won’t do you any good to choose an exercise that’s good for you, but you hate and avoid doing regularly enough to benefit from it. I no longer enjoy spending time in a gym pumping iron. However, I love backpacking so much that it drives me to do intensive strength training 3 times a week to make sure I have the various muscle groups in my body well-toned to keep me strong out on the trail. I also balance the strength work with 4 days of cardio workouts that include indoor or outdoor cycling at least once a week, elliptical or trail running at least once a week, and the other 2 days are more of the same or hiking/walking on trails to add variety and challenge my body in different ways. You will never see me in the pool swimming, or on the courts playing tennis or pickle ball… I just don’t enjoy it.

As I said earlier, find the exercise that YOU like and go for it!

Coming Next: The Four Pillars of Alzheimer’s Prevention - #4 Spiritual Fitness

Peace my Friends and Thanks for Reading!

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That’s right… your living habits can help you PREVENT Alzheimer’s Disease! Forget about those ads for miracle supplements, they don’t exist. You are your own best weapon, or your own best enemy, in the battle against AD.

Subscribe now

Numerous studies show the relationship between lifestyle choices and AD. The FINGER study in Finland of ~1,200 people over two years proved that a mix of healthy diet, regular exercise, social activities, and mental challenges can greatly reduce AD risk in people already vulnerable. Additionally, the MAPT study in France found similar results, showing that lifestyle changes across multiple areas can cut risk factors.

These findings match the “four pillars” approach promoted by groups like the Alzheimer’s Research & Prevention Foundation and the Alzheimer’s Association which found that the secret to prevention is connections. Brain connections (keeping your brain cells active and healthy), social connections (staying engaged with other people), lifestyle connections (eating well, exercising, and stimulating your mind), and emotional connections (maintaining psychological well‑being and balance).

Healthy daily choices like good food, movement, socializing, and mental activity can protect your brain and even slow decline. There’s no cure yet for AD, so prevention is about staying connected to your body, your mind, and the people around you. Even small changes in daily habits can make a big difference.

Leave a comment

Pillar 2: Stress Management

Stress is useful in emergencies, but harmful when it’s constant in daily life. Ongoing stress can damage genes, trigger inflammation, and raise the risk of AD. Since modern life is fast‑paced and stressful, it’s important to find regular ways to calm the brain.

When you’re stressed, your body releases adrenaline and cortisol in response. They cause your heart to beat fast and give you that buzzed or jittery feeling you get when stressed.

Cortisol is a natural response, but in excess, it messes up the way your brain metabolizes glucose and blocks your brain’s neurotransmitter functions, both of which damage your brain cells. Consistently high levels of cortisol also result in short-term memory loss. That’s why in very stressful situations you black out on details afterward.

There is a high correlation between three key physical conditions and the onset of Alzheimer’s disease. These conditions are high blood pressure, high cholesterol, and high cortisol. Not surprisingly, stress plays a significant part in all three. Recognizing and managing stress is a crucial part of any AD prevention strategy.

One approach for stress management uses Kirtan Kriya (KK) Meditation, which is a is a simple meditation practice that takes only 12 minutes a day. It involves sitting upright with a straight spine and resting your hands on your upper legs with palms up. Then singing the sounds “Saa Taa Naa Maa” while touching your fingertips to your thumbs in sequence (index, middle, ring, pinky… called mudras). This combination engages multiple brain regions at once, auditory, motor, linguistic, and memory circuits. That’s part of why it’s been studied in cognitive health research.

The chant is a sequence of primal sounds from the Sikh and Kundalini yoga traditions. Each syllable represents a stage in the cycle of existence:

Together, they describe the continuous cycle of creation and change. Not just biologically, but emotionally, psychologically, and spiritually.

People often describe the mantra as a reminder that everything is always in motion, change is natural (not threatening), renewal is built into the fabric of life, and we’re part of something larger than our individual story. It’s a way of stepping out of linear time and into cyclical time. A perspective that can be grounding, especially during periods of uncertainty or transition.

Long‑term practitioners often have larger, healthier brains and modern research shows KK reduces stress and boosts blood flow to brain areas important for memory and focus. Furthermore, studies found that KK strengthens brain regions that control stress, memory, planning, and organization. KK can also reduce anxiety and stress, slow or reverse memory loss in people with early decline, lower inflammation in the body, boost telomerase (an enzyme that protects DNA and supports long life and sharp thinking) by 43%, improve brain cell connections, and keep the benefits lasting for months.

KK is so practical as a stress prevention action because it takes only 12 minutes daily, no equipment or expensive training is needed, and it’s safe and has no side effects. You can use a recording on Spotify to help you get the rhythm down, it’s a “song” by Nirijnan Kaur called Kirtan Kriya (Short Version). The link will take you to it on Spotify and there’s a long version too which is 30 minutes of meditation. There are also smartphone apps for both Apple iOS and Android. On iOS it’s called “Kirtan Kriya” and on Android it’s just called “Kriya”.

Ironically, when I used to run far more than I do now, I’d get in my zone out on the road by making the same mudras with both hands simultaneously while I ran. I found it oddly peaceful and allowed me to focus inward on my body while running. I have no idea where the idea came from, I just started doing it one day and found it very centering.

I’m just a beginner with KK, so I don’t have a lot of insight to share personally yet. The mudras take a conscious effort right now for me, where when I’m running its subconscious. The softer the chant, be it sung out loud, whispered or silent, has a different effect on me in terms of energy versus calm. For a simple mediation, there is much to understand internally.

For years I have used a method called meditative or abdominal breathing to calm my body and thoughts. It’s so relaxing for me that I frequently doze off momentarily while doing it, so I use it to get to sleep when my mind is racing. The exercise is simple, take long slow breaths of equal length inhaling and exhaling. Place one hand on your heart and the other on your abdomen to center your mind on the beating of your heart and the rising and falling of your abdomen as you breathe. While slowly exhaling, notice the relaxation spread throughout your body. I prefer to do it while lying down, but I’ve also done it while sitting in a chair when I need to relax and don’t have the option of reclining.

This meditation can be set up in your Apple Watch using the “Mindfulness” app to bring consistency and depth to your breaths while you’re learning. I don’t know if an Android watch has something similar. I have my app set up for a 5-minute duration, and 5 breaths per minute, so that the breaths are long and slow. The watch has haptic signals (vibrating) to guide you through breathing in and out so you don’t have to watch or listen to anything which would defeat the purpose.

It’s the only meditation I have ever used that allows me to block out the world and calm my mind and thoughts (I’m not here yet with KK). Even though I can’t wear a watch during MRIs, I use the same concept during them to calm me and block out all the noise of the machine. I also take advantage of the time in the infusion chair to do this quietly and the nurse is always surprised that my blood pressure is considerably lower when I’m done than when I begin.

These simple stress management methods are easy to use for both caregivers and patients regardless of mobility. Both patients and caregivers need to be mindful of self-care and alleviate stress!

There are many smartphone apps available like Calm, Mindfulness, Mindfulness.com, and Mindfulness Coach. I looked at them, but for me I didn’t see the value. They have annual subscriptions ranging from $60 to $130 for anything beyond the most basic options. Check them out and make your own decision.

The bottom line is chronic stress harms the brain, but a short daily practice like KK or abdominal breathing can lower stress, improve memory, and protect against Alzheimer’s. They’re simple, safe, and powerful. I’ve only showed you two stress reduction exercises, but many other simple approaches including meditation, yoga, prayer, and others can have similar positive effects.

Coming Next: The Four Pillars of Alzheimer’s Prevention - #3 Exercise

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It’s December 27, 2025, and I’m still me. 😊 It’s now been 4 months since my diagnosis. As I look back on 2025, I’m really settling into a new normal and I’ll be moving to monthly progress posts for my personal experiences. All other deep dives on informational topics I’ve come up with will continue as I complete them.

I’ll also happily take special requests you send me to dig into. So… if you have an Alzheimer’s topic you’re dying to know about, let me know and I’ll research it and publish an article!

It’s smack dab in the middle of the holiday season and I am once again reminded of what I’m fighting for. My family is around me, and my most amazing wife and partner Jan is a rock of support for me! I’m a lucky guy (aside from the Alzheimer’s thing of course).

My lecanemab treatments are still going well. Two months of the bi-weekly infusions are behind me, and 16 more months (32 infusions) to go until I move to maintenance mode. My second ARIA MRI is in 3 days and I feel good so I’m not worried about it. I’ve had some headaches lately, but I’ve had frequent headaches for years, and over the last few months they’ve actually been less than usual.

I had a set of routine bloodwork done this week and didn’t expect anything out of the ordinary. Given how this year is going, I should have expected something else to pop up. I found out that I’m now considered to be in pre-diabetes territory. I’ve read that it’s common for AD patients to have higher fasting blood glucose levels that push into the prediabetic range. As a result, I’m going to change my diet to cut way back on empty carbs, and when I do eat them, I’ll focus on high fiber carbs. The other things they recommend for controlling blood sugar I already do. I exercise a ridiculous amount, I eat much more home cooked foods than processed foods, and I avoid sugar. I do admit, for the last 6-9 months my carb consumption has been higher than usual, and my diet worse from the stress of seeking answers and then actually getting the one I didn’t want. Time to dial it back!

I proved to myself the last few weeks that I can still handle action-packed times like I used to. Whew what a whirlwind few weeks its been! We helped our daughter and future son-in-law settle into their new apartment. I completed the work in their network patch panel to light up all the ethernet ports in the rooms that the building owners never did. I hadn’t done network patch panel wiring in a decade, but it all came back! I’m also taking an online course in AI prompt writing, which is very helpful to me when doing research on AD topics. Plus, my Master Naturalist program is ramping up. This past weekend we spent a day learning about birds and simulating a Christmas Bird Count at the Sharon Audubon Center. Now that I’ve developed my phenology project for the course, I’m doing the data capture & observation work weekly to develop a 12-month analysis. I know you all are just dying to know what my project is, but you’ll have to wait like everyone else until it’s done next November… 😜

My wife Jan and I have always dreamed of visiting Antarctica and this week we actually booked an adventure cruise to Antarctica in 2027!!! We are SO excited, because we’re going with my sister and her friend as well! What a special trip to go on with both my wife, and my sister whom I’ve always been so close with. We’ll be travelling to the southernmost city in South America, Ushuaia, Argentina. There we’ll board a small ship, sail across the infamously turbulent Drake Passage where the Southern, Atlantic and Pacific oceans meet. We’ll sail to the Shetland Islands north of Antarctica, travel down the coast of the Antarctic Peninsula and cross the mythical boundary of the Antarctic Circle before heading back. While there we’ll be camping overnight on the continent itself, kayaking frequently through the sea ice and along the shore, and exploring by snowshoe. It’s not a luxury trip, it’s an exploration trip where we can also participate in citizen science projects which I will absolutely be doing to help document the impacts of climate change!

I’m slightly concerned that once I’ve disclosed my AD diagnosis the cruise line might hesitate to allow me to go, so I’ll be getting doctors letters in order to bolster my case. These scenarios are where people who don’t understand the disease, may handicap me needlessly when in reality, I’m a more experienced and competent explorer than most who will be on the ship.

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The next year or so is going to be very adventurous! While together for the holidays, our family decided to take a trip together. We all suggested places and decided on Portugal! I enjoy trips with our children and their spouses so much because it’s time for us to spend relaxing, exploring, and enjoying each other’s company for a week straight. In some families that might be torture, but we enjoy being together (I think) and I wouldn’t miss these opportunities for anything. We’re now going to start planning out what we want to do while there and since we all enjoy history, hiking, and relaxing, I’m sure there will be plenty of each! Well, maybe not so much relaxing…

As I leave a pretty brutal 2025 behind, and look forward to 2026, I’m filled with contentment and hope. What a joy it has been to have my family around me for the holidays! I’m so very blessed and thankful for their love and caring. I’m also grateful for my friends that I don’t see as often, but when we do reach out to each other it’s like we were never apart. And I’m thankful for you, my readers, who encourage me and keep me writing! You all are what gets me up each day, you pick me up when I’m struggling to find hope, and you somehow know just when to reach out and check in with me when I need it.

Coming Next: The Four Pillars of Alzheimer’s Prevention - #2 Stress Management

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It’s December 13, 2025, and I’m still me. 😊 Wow what a crazy busy start to December and the holiday season!

I got my stitches out from my skin cancer surgery. It wasn’t a big deal and it felt SO good to get those steri-strips off my cheek! They were so close to my eye that I could feel them every time I blinked. Surprisingly the incision looks quote good already and the doctor says it’s healing nicely and won’t leave much of a scar. At some other point in my life, the thought of a scar on my cheek would have annoyed me, but I have far bigger fish to fry than worry about that. In reality, I’m disappointed I won’t have a scar because now I can’t continue to use my story I cooked up about having to fight off a bear while backpacking in the woods! 😁

Despite still being me, feeling great, and being extremely active, I have to admit that I feel what I’m sure every person with AD feels. Not a day goes by where I don’t think about my disease in some way and more often than not it makes me fearful or anxious. Every time I go downstairs and forget what I went down for, or blank on someone’s name, I think … “Is this a sign the disease is progressing?” It’s likely akin to a cancer patient who worries that every pain might indicate their disease has returned. Someone who doesn’t have it can’t relate because it’s totally irrational, but anxiety isn’t rational and fear isn’t rational. So, we have to acknowledge the monster lurking, but try to push it back into the closet for another time, and get back to our lives.

Speaking of getting back to our lives and being active… I started my new Master Naturalist certification program being run by the CT Forest & Parks Association. It’s a yearlong certification program where we learn about plant phenology, aquatic species, birds and animals of New England. The goal is for us to first learn, and then use our knowledge to go out and spread the word with others through community service, teaching, and speaking. If we help others gain an understanding, love and respect for nature, then maybe they’ll join us in trying to protect it from destruction due to greedy corporate expansion & pollution. It’s a similar program to the Master Woodland Manager certification program I completed in 2024. We spend a day a month wandering the woods and fields, and another evening a month in virtual classes learning and sharing. We also have to complete 30 hours of service as a naturalist, and attend 4 more educational events of our choosing, and complete a yearlong phenology project in a natural setting of our choosing. I have to work hard to keep up with my classmates because many are professional biologists, and land trust managers so much of this is already lived experience for them. I’m up for the challenge though! Okay, maybe not for the first virtual class we had recently… I neglected to read all the emails and hadn’t completed the assigned reading so I was totally unprepared for the discussion. That won’t happen again!

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The anxiety I mentioned earlier comes in many forms. I had my first mid-treatment ARIA MRI this month… If you don’t remember from earlier posts, for patients like me receiving lecanemab or donanemab infusions to slow the progress of the disease, we are at risk of a condition called ARIA (Amyloid Related Imaging Abnormalities). Essentially our brains can swell dangerously or we can experience micro-bleeds within our brains because the drug has a hard time crossing the blood-brain barrier. So… they do 4 MRIs early on to see if this is occurring. One after 2 infusions, one after 4 infusions, one after 6 infusions, and one after 12 infusions. If I don’t have any evidence of ARIA by then, I’ll continue treatments without regular MRIs. I’m already considered low risk because I don’t carry APOE e4 gene but it’s better to be safe. That’s a LONG lead up to saying that I had the MRI and it was clear, yaaaay!

To be honest, I wasn’t worried about ARIA because I have had ZERO side effects, no headaches, no nausea, no sleepless nights, zilch. What I was worried about was disease progression … this is pure irrational anxiety … a few days before the MRI it occurred to me that if they do an MRI they may notice that my brain size has shrunk or white matter has decreased. OMG I could find out that I’m getting worse! I know, that is silly, AD doesn’t progress so fast that you notice changes like that in one month, but I was anxious going into it and was worried to hear the results afterward. In the end, it showed no progression, but I’m sure that won’t stop me from being anxious leading up to the next ARIA MRI as well.

I had my third lecanemab infusion, and they are going great! We’ll as “great” as it can be to get an IV every two weeks. I wondered whether they’d have to find a new vein each time and eventually my arms would look like those of a drug addict’s. Not to worry, our veins heal fast and the nurse uses the same one each time. I have to say, I’m thankful that I have GREAT veins! 😊 I have low body fat, so my veins naturally pop up out of my hands and arms which give them a really nice target. 🎯

I’m sharing my AD diagnosis with more people now and it gets easier to talk about each time. I have leadership volunteer roles with several nonprofits, so I wanted to make sure I spoke to each of their CEOs before I announce my diagnosis publicly and assure them that I have no intention of stopping my work with them any time soon. As usual, their responses have been wonderful, compassionate, caring and supportive! Each conversation I have encourages me to be more open because people are so supportive. I also pay attention afterward to see if people drift away from reaching back out to me or communicating with me and I’m not seeing it. For those of you whom I’ve spoken to already, I love you for your support and for not abandoning me. For those whom I don’t know, please be equally supportive if a friend, co-worker, or family member reaches out and shares with you. We NEED your love and support!

Coming Next: End of year reflection

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That’s right… your living habits can help you PREVENT Alzheimer’s Disease! Forget about those ads for miracle supplements, they don’t exist. You are your own best weapon, or your own best enemy, in the battle against AD.

Numerous studies show the relationship between lifestyle choices and AD. The FINGER study in Finland of ~1,200 people over two years proved that a mix of healthy diet, regular exercise, social activities, and mental challenges can greatly reduce AD risk in people already vulnerable. Additionally, the MAPT study in France found similar results, showing that lifestyle changes across multiple areas can cut risk factors.

These findings match the “four pillars” approach promoted by groups like the Alzheimer’s Research & Prevention Foundation and the Alzheimer’s Association which found that the secret to prevention is connections. Brain connections (keeping your brain cells active and healthy), social connections (staying engaged with other people), lifestyle connections (eating well, exercising, and stimulating your mind), and emotional connections (maintaining psychological well‑being and balance).

Healthy daily choices like good food, movement, socializing, and mental activity can protect your brain and even slow decline. There’s no cure yet for AD, so prevention is about staying connected to your body, your mind, and the people around you. Even small changes in daily habits can make a big difference.

I’m going to share the Four Pillars in four separate articles, beginning with Diet & Supplements to make it more digestible (pun intended 😁)

Pillar 1: Diet & Supplements

The relationship of diet to brain health is clear. The typical American diet is heavy in empty calories including processed foods, sugar, salt, and unhealthy fats. All are linked to higher AD risk. Worse yet, processed food manufacturers have developed what they call the “sweet spot” to feed to unsuspecting consumers which is just the right mix of salt, fat and sugar to make you want to keep eating, and come back for more again and again.

A plant‑based diet, which consists of lots of fresh vegetables, fresh fruits, nuts, seeds, legumes, and whole grain foods, doesn’t create unhealthy cravings, helps protect your memory, and may even slow or reverse cognitive decline. The well-known Mediterranean diet that prioritizes vegetables, fruits, olive oil, nuts, and fish/seafood has strong ties to better brain health. People committed to the Mediterranean diet show fewer AD-related plaques and tangles accumulating in their brain, and they have a thicker brain cortex in memory areas, instead of thinning seen with the typical American diet.

The MIND diet, which is a mix of the Mediterranean and DASH diets, can make your brain act up to 7.5 years younger. The MIND diet recommends 9 “brain healthy” foods to include, and 5 unhealthy foods to avoid.

• The healthy items include:

  • 3+ servings a day of whole grains (oats, quinoa, brown rice, buckwheat, amaranth)

  • 1+ servings a day of vegetables (other than green leafy)

  • 6+ servings a week of green leafy vegetables (kale, spinach, etc.)

  • 5+ servings a week of nuts (tree nuts)

  • 4+ meals a week of beans (beans, lentils, soybeans, peanuts)

  • 2+ servings a week of berries (straw- blue- rasp- & blackberry)

  • 2+ meals a week of poultry (chicken & turkey)

  • 1+ meals a week of fish (salmon, trout, tuna & mackerel)

  • Use olive oil if added fat is needed

• The unhealthy items which are higher in saturated and trans-fat, and their recommended dietary consumption are:

  • Less than 5 servings a week of pastries and sweets

  • Less than 4 servings a week of red meat (including beef, pork, lamb, and products made from these meats)

  • Less than 1 serving a week of cheese and fried foods

  • Less than 1 tablespoon a day of butter/stick margarine

The Alzheimer’s Research & Prevention Foundation’s Nutrition Plan highlights a similar approach. Fresh juices provide vitamins and nutrients that support brain strength, and supplements like omega‑3 oils, CoQ10, resveratrol, and a strong multivitamin may also support brain health.

Genes vs. lifestyle in AD causation is often misunderstood. While genes can raise Alzheimer’s risk, diet and lifestyle influence how those genes act. The key takeaway is that genetics are not our destiny, healthy eating can shift the odds toward a sharper brain.

Switching from a processed, meat‑heavy diet to a Mediterranean or MIND‑style diet that’s rich in plants, healthy fats, and nutrients offers one of the best ways to protect your brain and reduce AD risk.

Note: I went headlong into the MIND Diet and was initially unsuccessful. It can be a big shock to your digestive system, and it makes sense to work your way into it over many months. I’ve been eating lots of fresh vegetables and fruit for many years so that part was already taken care of. Removing some of the empty carbs like potatoes, corn & rice, and corn/rice-based foods since I also try to keep gluten-free was difficult because I love carbs, but I did it. However, adding so much fiber and healthy fats back into my diet from legumes, seeds, and nuts was very impactful. I loved them all but my gut biome was overloaded. I don’t want to be too gross here, but I got uncomfortably gassy and my very predictable bowel movements became very unpredictable. I decided to back off, and I’ll try reintroducing different components to my diet much more gradually once I get my digestive system restabilized. Too much of anything, especially rapidly, can be challenging to our systems.

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Nutritional Supplements

People are willing to collectively spend billions of dollars a year on “nutritional supplements”, most of which have no medical evidence that they improve our health, and some even cause serious issues. The ones that are heavily marketed as “brain” and “memory” improvers are nothing more than empty claims that give you a good dose of B-complex vitamins to provide a niacin flush or caffeine to give you a jolt of jittery energy, but they do nothing to improve your memory or brain function. So many people waste their money on promises of a miracle cure … spoiler alert, there is none.

I’ve come to learn that the highly marketed “cocktails” of various vitamins, minerals and extracts that are sold as memory boosters are crap. I decided to focus my search on basic supplements, and found that there are a few which have potentially legitimate claims of positive impacts on brain health that I’ll discuss because not all that have promise pan out to have real cognitive benefits:

Probiotics: A healthy gut has a strong correlation to a healthy brain, and probiotics are an important part of maintaining a healthy intestinal biome. I spoke with my GI doctor about what I could expect in terms of digestive issues as a result of AD and he took the opposite approach and talked to me about the positive gut-brain connection. In addition to good eating habits like the MIND diet, he said probiotics are important to maintain balance in our guts and he recommended the one probiotic that is actually FDA approved, it’s called VSL #3. You can tell this company is great at product development but not marketing… their products are named VSL #3 and VSL4. 🤣 I’ve used probiotics before, but this one feels different. In investigating these, I learned that probiotics lose their potency when they sit out at room temperature and when they are processed to be able to sit at room temperature. VSL #3 is shipped in a box with cold packs and you have to store it in your refrigerator. The capsules can be kept at room temperature for a maximum of 2 weeks so you can take them with you on a vacation without loss of potency. I also learned that probiotics also lose their potency if you take them with hot beverages or food, so I get up in the morning and take them with ice cold water, eat my plain Greek fat-free yogurt with fresh raspberries and blueberries, and wait 30-60 minutes before having my morning tea. I found that the best price for this is buying directly from their site, getting the four-pack, and using the auto-ship discount.

Omega-3 Fats can be found in many fish and nuts as well as supplements are proven to be beneficial for your heart and brain health. Some of the best food-based sources are salmon, mackerel, sardines, herring, flax seed, walnuts. Fish offer the most beneficial forms of Omega-3 (EPA and DHA) and if you’re not a fish eater, Omega-3 supplements are available. I love to eat fish, but my family will only put up with so much fish in our diet. Two things to be careful of:

1. Plain fish oil capsules can make you burp a nasty fish taste which I can attest to.

2. Omega-3 extracts are best from small fish (anchovies, sardines, herring, mackerel) so pay attention to the label. The larger the fish (king mackerel, tuna, swordfish), the more toxins they accumulate in their bodies from what they eat.

I like a particular brand called Spring Valley Maximum Care Omega-3 and I take 2,000mg per day with no fishy after taste!

Vitamin B3, or more specifically a derivative of it called Nicotinamide Riboside (NR) has some outlandish marketing claims by some supplement companies of being able to reverse the effects of dementia, which we all know is impossible. However, more modest claims about the derivative have some encouraging validity.

NR is proven to boost NAD⁺ in your brain, a molecule your cells rely on for energy and repair. That’s good for overall brain resilience, but there isn’t yet human evidence that NR improves cognition or slows Alzheimer’s. Think of it as cellular support to help with energy metabolism, repair, and inflammation support, all of which are issues in the brains of people with dementia. It is not a cognitive treatment.

I volunteered last fall to participate in clinical trials with the Massachusetts General Brigham medical center’s research group to test out the beneficial effects of NR. While I wasn’t able to participate since I’m receiving lecanemab treatments, they shared the information with me in case I wanted to begin taking it on my own. I checked with my primary care physician (PCP) who said it was fine and I’ve been taking it since early January. They say that 3-4 weeks is about the timeline needed for it to start having any positive effects (if any) so we’ll see if I notice anything. I investigated this extensively once I applied for the trial and could write an article just on this one because there are so many crappy offerings out there and poor quality manufacturers. Lots of companies mix it with crap fillers and offer bougie cocktails that are a waste of money. There are at least three forms of it that are marketed, nicotinamide riboside chloride, liposomal nicotinamide riboside, and nicotinamide riboside hydrogen malate. If you’re interested in taking NR, reach out to me and I’ll share more about how to choose a supplement. I spent a lot of time ferreting out the best one at the optimal price point.

Lion’s Maine mushroom extract is a questionable but harmless one. There are lots of claims of its benefits in relation to cognition and brain health. I spent a lot of time seeking out a quality supplement to try and liked what I saw from RealMushrooms which offers down to earth (pun intended 😁) mushroom extracts from organically grown fungi without all the fillers, pesticides and other crap . In the end I found no tangible value in taking it for 6 months a few years back. Others claim to have had measurable positive effects. I try to eat more raw mushrooms of all types now because they do have health benefits, but it’s not as a dementia solution.

Creatine has long been rumored to benefit athletes in the building of lean muscle mass and when I was younger and training intensively to build muscle and stamina for road and trail racing, I used it; but I didn’t notice any benefits. More recently it has been linked to cognitive improvements for people who are sleep deprived, highly stressed, on low-creatine diets (vegan & vegetarian), or are older adults. The potential benefits of taking it for older people are that it may improve short term memory and mental fatigue, and it has possible neuroprotective effects. These claims have not been extensively clinically validated.

There is growing evidence that lithium may be a key supplement in brain health. There are decades of research on lithium because of its use for treating various neurological disorders like bipolar and major depressive. Emerging studies suggest that at the right doses and in the right scenarios, it may support brain resilience, neuroprotection, and long‑term cognitive health. There are clinical trials using it to treat AD and MCI but no results are available. Lithium Orotate is the most common nutritional supplement form, but I won’t go any further than that on lithium because Lithium can interact with medications and affect kidney or thyroid function so be sure and consult with your doctor before starting to take it.

Resveratrol is one of the supplements recommended by the Alzheimer’s Association as part of a brain healthy diet. Resveratrol has interesting theoretical and preclinical cognitive benefits, but human evidence is weak, inconsistent, and often disappointing to date. It’s far less convincing than creatine, NR, or even low‑dose lithium in terms of real‑world cognitive impact. It might help by reducing oxidative stress and inflammation, increasing psychomotor speed in older adults, and improving metabolic health, but we must take the clinical promise with a grain of salt because the few studies performed to date have showed disappointing real-world results from taking 1,000mg a day.

Finally, Coenzyme Q10 (CoQ10) is another supplement recommended by the Alzheimer’s Association as part of a brain healthy diet. Tests have shown that it has little effect on prevention, and is more beneficial to people who already have cardiovascular and neurological issues. It shows some cognitive benefits in human tests, but the results are too inconsistent to call it a reliable cognitive enhancer. CoQ10’s most plausible benefits are supporting cellular energy efficiency in aging brains, reducing oxidative stress, and improving cerebral blood flow.

Supplement Summary

Here’s a supplement summary matrix I created to simplify all that information you just read…

• Most powerful for neuroprotection: Lithium

• Most reliable for situational cognitive performance: Creatine

• Most promising for cellular support: CoQ10 and NR

• Most overhyped relative to human results: Resveratrol and Lion’s Maine Mushrooms

Note: Never start taking a nutritional supplement without having discussed it with your PCP. They can counsel you on any possible side-effects or interactions with other medications you may be taking.

Caution: All nutritional supplements are NOT created equal. Some are poorly controlled and have been found to have dangerous levels of lead and other toxic substances in them from shoddy manufacturing processes. Others don’t give you the dosage claimed and instead add fillers. Never buy a nutritional supplement that hasn’t been independently analyzed by a third party lab, and always download & read that analysis! I downloaded one recently and when reading it I discovered that the 3^rd party performing the analysis was the same 3^rd party that was manufacturing it … if that isn’t “the fox guarding the henhouse” I don’t know what is!

Coming Next: Weeks 15 & 16 Update

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It’s November 28, 2025, and I’m still me. 😊 Every week feels better now, I feel like those dark days of August and September are behind me and I finally have my life back on track. I sleep great, I’m upbeat, and I’m re-engaging in all the things I had withdrawn from for a few months. Life is good … except for the fact that I have Alzheimer’s Disease lurking in my brain waiting to pounce. For now, it’s “game on” for the rest of my life!

After months of waiting, I finally had my first meeting with a new doctor from Yale University’s memory disorders clinic. It was as wonderful of an experience as you can have when going for an Alzheimer’s clinical examination. For you “older” readers, my wife Jan described him as “Marcus Welby,” a TV doctor who was compassionate, knowledgeable, and supportive. He added a great write up to my healthcare profile that provided lots of hope and positive insight. Here are some excerpts of a note he wrote to my primary care provider who had personally worked to get me into the clinic for evaluation …

Dear Dr. XXX, Thank you for allowing me to evaluate your patient, Mr. Scott Redfern at Yale Memory Clinic on …, for complaint of memory deficits. … He is complaining of occasional forgetfulness. … There is no significant change in his ability to remember names, and he does not repeat conversations. He recalls recent activities, including strength training and receiving his first lecanemab infusion, with no side effects noted. … He is able to perform basic activities of daily living, including driving, exercise, contributing to household living and finances.

Assessment & Plan: Alzheimer’s disease with mild cognitive impairment. … Continue lecanemab infusions. <listed diet & activity dos & don’ts> Keep safe and active. Follow up in 6 months.

I discussed diagnosis, treatment and prognosis with patient and his wife … a total of 55 minutes was personally spent by me. This does not include any resident/fellow teaching time, or any time spent performing a procedural service.

I didn’t share this because you need to know my doctor’s assessment, I shared it because this is what a healthcare practitioner should be capturing and putting into a patient’s record! He also included a picture of the MoCA (Montreal Cognitive Assessment) test he administered showing how I performed on each section and how he scored it. I found it very thoughtful that he took the time to respond personally to my PCP about my assessment. Lastly, I love how he kept track of how much time he personally spent with me, and the vast majority of that time was face-to-face, not writing up paperwork in the back room. That’s the type of care we all deserve!

I’ll contrast this supportive experience to my current neurological practice I’m working to move away from where their writeups are mechanical and look like a cut and paste from a billing key, their assessments are regularly missing critical test results that I have to ask for repeatedly, MoCA test results are simply a score with no backup (because they don’t actually administer a full MoCA test), and they include assessments they performed months ago - not in that visit (maybe to claim more time for billing). Every visit with them feels like a financial transaction, not a healthcare evaluation and strategy discussion. When the time is right, I’m outta there.

I went up to Massachusetts to see my parents and my aunt, and had decided that this would be the day I’d tell them about my diagnosis. My mom has finally nearly fully recovered from a bad fall 3 months ago, so this won’t be adding undue stress to an already stressful recovery process for us all. Just like the conversation with my children, I had enough information to give them a full story of diagnosis, progression, treatment, and prognosis. Like the conversation with our children, this one went well too. My parents and aunt asked many good questions and were very supportive of my treatment plan and approach, and of course they were concerned for how my family was handling the news, especially my wife Jan. I worried about it being very emotional, and I got a bit teary when answering the question about how my family was handling it, but overall since I feel I’m in a good place at this moment in time, it was easy to be positive without being disingenuous.

My second lecanemab infusion occurred without incident and the first week of December I’ll have my first MRI to make sure that no ARIA (Amyloid Related Imaging Abnormalities) is occurring as a result of the treatment. In human-speak, ARIA is stuff that shows up on an MRI indicating a bad reaction to the medicine like swelling or bleeding in the brain. I discuss this condition in detail in prior articles like “Alzheimer’s Disease Treatments”. My risk is very low, but it is an FDA requirement to get periodic MRIs in the first 6 months to ensure that this is not occurring. After 6 months, if I haven’t experienced it, the likelihood of it occurring is even less. I haven’t had headaches, nausea or other symptoms that indicate ARIA might be occurring so I feel confident!

Cat therapy: Video of Gilligan “helping” me change the sheets

Two months ago when I was “wandering in the desert of despair,” one of the test results I was anxiously waiting for was the biopsy for skin cancer on my face. It came back as malignant, and I recently went in for surgery to have it removed. I was stressed because it was right under my eye. The surgery was with local anesthetic so I wasn’t looking forward to seeing a scalpel working so near to my eye. The Mohs procedure also requires multiple progressive excisions to take out as little tissue as possible to minimize scarring, while ensuring all cancerous cells have been removed. The doctor was a real hoot, she never stopped talking and that was great because it distracted me. We talked about her daughter in college, the perils of AI (artificial intelligence), and when I asked if this surgery or the sutures would jeopardize my upcoming MRI we got into a protracted discussion on AD. I have to say, I love being able to talk about my diagnosis now, have people ask me questions without fear of emotionally wounding me, and discuss it casually. I have the disease, I accept that, and I’m going to talk about it as nonchalantly as possible … it’s one of my new passions to help make it more acceptable and less taboo!

I’ve also begun to tell former co-workers, friends & other relatives whom I don’t want to be surprised by a social media post when I launch this new Substack space. For the most part, they have been amazingly supportive, inquisitive, and unphased. A few seem uncomfortable or unsure of what to say, but that’s very understandable. I have faith that they will all surround me with support and friendship rather than pulling away due to discomfort.

I mentioned in an earlier post that I have signed up with both Yale University’s and Mass General Brigham Medical Center’s memory disorders clinics to participate in new trials for leading edge treatments for AD. Two new opportunities came up at Yale that I plan to investigate further. They both are focused on reducing the level of tau protein tangles in an AD patient’s brain. The reason why the lecanemab treatments I’m getting are only mildly effective, is because they only address half of the problem in my brain. Lecanemab reduces formation of amyloid plaque, but does not address tau tangles which are thought to have an even greater impact on the destruction of neurons and brain cells. If it’s not too intrusive, and they determine I qualify, I’ll consider participating. As I’ve said before, I’m leaving no stone unturned in this war!

Coming Next: The Four Pillars of AD Prevention - Pillar 1: Diet

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When we talk about federal healthcare research funding, we’re really talking about giving hope. Hope for people like me with Alzheimer’s disease (AD), as well as families dealing other devastating diseases like cancer, Parkinson’s, ALS and countless other conditions. Hope for breakthroughs that can transform lives, and hope for a future where prevention, treatment, and even cures are within reach.

For decades, the US has led the world in biomedical research, largely because of sustained investment in the NIH and related programs. This funding doesn’t just fund laboratories, it fuels innovation, trains scientists, and supports clinical trials that bring discoveries from labs to people desperate for a cure.

In the realm of AD, federal funding has enabled landmark advances in research, from identifying genetic risk factors to developing drugs that target amyloid and tau proteins. Large-scale trials funded by the NIH have explored how diet, exercise, sleep, and social engagement can reduce dementia risk. These studies have been essential because they translated science into everyday actions for us to take while awaiting a cure. My doctors keep telling me that this is a time when AD research and treatment is progressing faster than ever before, but when I ask them about the federal research funding cuts, they also admit that much of that promise is at risk.

Programs funded by the NIH also provide education, early detection strategies, and caregiver support across communities. Programs like the Healthy Brain Initiative (passed in 2005) and BOLD Infrastructure for Alzheimer’s Act (passed in 2024).

Let’s get more specific though for you data geeks… the NIH is currently funding hundreds of AD research projects, with some of the most crucial trials focusing on early detection, prevention, drug development, and lifestyle interventions. Here are some of the most notable statistics and examples:

• The Ahead Study which focuses on treating AD before memory loss begins. It uses PET scans and blood tests to detect amyloid buildup in symptom-free volunteers, then tests whether antibody drugs can clear amyloid and prevent disease onset. The potential is for it to lead to preventive therapies, like a pill taken daily, that stops AD before it starts!

• Biomarker Development Trials focus on identifying microRNA biomarkers in blood to classify stages of neurodegeneration. Its potential is to offer non-invasive diagnostic tools to detect Alzheimer’s early and track progression.

• The National Institute on Aging (NIA) is currently funding 495 active trials across AD and related dementias … WOW! … including:

  • 68 trials testing therapies like anti-amyloid (e.g. lecanemab & donanemab), gamma secretase modulators which modify the way the enzyme breaks up amyloid proteins, and glutaminyl cyclase inhibitors which blocks the process that makes amyloid proteins sticky and causes them to clump.

  • 157 trials exploring lifestyle factors (diet, exercise, sleep, cognitive training).

    217 trials focused on caregiver support, care models, and community interventions.

  • 19 trials developing advanced tools for early detection.

  • 31 trials studying the biology of AD and related dementias.

• The VIVA-MIND Trial focuses on testing a small molecule inhibitor (glutaminyl cyclase) to reduce the buildup of harmful amyloid protein clumps and harmful chronic inflammation in the brain in adults with mild cognitive impairment (MCI) or early AD. The potential for this treatment is to slow the disease’s progression in early stages.

You may have noticed that many of these are focused on prevention and early-stage treatment, which is so important to those of us either at risk or already in the early stages to buy us time for a cure, or at least a way to stop its progression.

Research in one area, for example Alzheimer’s disease, often sparks breakthroughs in other neurological conditions. Just as cancer research has advanced immunology and infectious disease studies, and diabetes medications have transformed obesity and weight loss.

In 2025, federal budget cuts slashed deep into the heart of NIH and related programs, up to 40% in some areas. For Alzheimer’s disease, the consequences are particularly stark:

• The hundreds of NIH-funded Alzheimer’s trials listed above could be delayed or canceled, halting progress on prevention and treatment strategies.

• Long-term studies like the Dominantly Inherited Alzheimer Network (DIAN), which track families with genetic risk, may lose critical support.

• Staff reductions have already hit initiatives that provide education and caregiver resources, leaving families more isolated.

• After years of bipartisan commitment to increasing dementia research funding, these cuts threaten to set progress back decades.

There is good news… in the recent budget funding for fiscal 2026 passed on February 3rd, Congress ignored the Trump administration’s request to further slash HHS and NIH funding and instead funded many crucial programs. That funding included an additional $100 million for Alzheimer’s programs, and $41.5 million in continued funding for the BOLD Infrastructure for Alzheimer’s Act in the CDC. That’s very encouraging news, but even that falls short of what is needed. Expert assessments have determined that in order for implementation simply to keep pace with the rapid progression of recent research, the NIH needed at least $110 million in additional funding and that doesn’t include catching up with what was lost due to Trump’s slash and burn approach to the NIH budget in 2025. The new funding did not include directed funding for staffing requirements, so given how many people were terminated across the CDC and NIH in the last year, funds are irrelevant if there is no staff to manage programs and award grants to researchers and clinics.

We, and Congress, must be vigilant about the new funding. The Trump administration has shown a complete disregard for Congressionally approved budgets, and has violated the law by cancelling approved projects. There is no guarantee this funding will ever translate to the intended implementation unless we hold them accountable through our representatives in Congress and our votes this fall.

Alzheimer’s is not just a medical condition; it’s a world-wide health crisis. An estimated 7.2 million Americans live with the disease today, as well as over 50 million people world-wide. Those numbers are expected to double in the coming decades as our population ages and environmental conditions exacerbate the problem. Every dollar cut (or unspent) for research and clinical implementation is a dollar taken from the fight against a condition that robs people like me of our memories, independence, and dignity as it progresses.

Federal healthcare research funding is not charity, it infuriates me when I hear ignorant people say that! Healthcare research funding is an investment in healthier communities, an investment in reduced healthcare costs, and an investment in the possibility of a future where AD and other devastating diseases are no longer inevitable and incurable. Most importantly, it’s HOPE for those of us living with, and battling it, and we desperately need hope to keep up the fight.

Budgets set the direction, but implementation determines the outcome. The people living with Alzheimer’s like me, and those who love them, are the ones who keep the system honest because we must in order to survive.

Progress isn’t inevitable, but it is possible when we insist that breakthroughs are followed up on, research is turned into clinical trials, and trials & treatment reach every community, not just the ones closest to research centers.

I’ll be even more blunt … for people like me, and your friends and family battling the disease, last year’s cuts set AD research back as much as a decade which could very well be a death sentence. The typical life expectancy of a person diagnosed with AD is 8-12 years. So in 10 years, many of us battling it today will have progressed to a point where we can’t return to our old selves, and nothing can change that. AD can’t be dialed back with a cure. Once brain cells are dead, and memories are gone, they’re gone forever … WE are gone forever.

As voters, advocates, storytellers, caregivers, and patients, we have to make our voices heard. Cuts to Alzheimer’s research funding, cancelling approved grants, and intentionally ignoring congressionally allocated budgets are not abstract. They affect real people, real families, real scientists, real progress, and they destroy real hope. Restoring and expanding federal healthcare research investment is essential if we are to honor our senior citizens who have given so much to our country and our communities during their lives.

Coming Next: Weeks 13 and 14 Update

Peace my Friends and Thanks for Reading!

Note: What I’m sharing in my deep dive newsletter articles is based on personal research, but please remember I am not in the healthcare profession, and I have no credentials in that area past or present. I’m sharing what I’ve learned, and will continue to learn, in my own desperate effort to advocate for myself when meeting with my care team. I believe everything I share to be correct or I wouldn’t share it, but you should not take anything I say as medical advice.

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It’s November 14, 2025, and I’m still me. 😊 It’s now been 3 months since my diagnosis. I thought by now that progress and learning would have slowed down and I’d quickly shift to monthly updates, but this period has been nonstop learning and progress! Maybe I’ll stick with bi-weekly updates until the new year. This was a period of big accomplishments: I scheduled my first lecanemab infusion, I went on a long backpacking trip, I applied for a new clinical trial, I met with a new neurologist, and we shared my diagnosis with our children.

I had the opportunity to go backpacking on the Laurel Highlands Hiking Trail with my two friends, Danny & Deb, which you can read about in a separate Substack post here. Every “normal” thing that I do reminds me that I am truly still me! I know not all of you may consider backpacking 20 miles a day with 30 pounds of gear on my back as normal, but it’s my normal and it was so amazing to get out and backpack with friends rather than just going solo. The more opportunity I have to share my diagnosis in person with people whom I care about, the better I feel. I know I can’t meet up with everyone and tell them live, which gives them opportunities to ask questions, but in the next few weeks after I’ve told my children, I will share with more and more people. Since I was with Deb & Danny for 4 days and 4 nights, I took the opportunity to tell them. Their reaction was exactly what I needed to hear! The fear with AD patients is that by sharing news of this disease, friends will melt away either because they don’t understand AD or because they now feel awkward being around you. We talked at length about my prognosis and how it affects me, and then they said the most wonderful thing to me … “we don’t care, we’re still going to drag your ass out backpacking with us!” I love you both for that Danny & Deb, thank you!

I got an email response to my application to participate in a new medical trial being conducted by Mass General Brigham Medical Center. It’s a 12-week study investigating the effects of Nicotinamide Riboside (NR), an over-the-counter Vitamin B3 derivative, to see what effects this supplement has on brain energy metabolism in those with MCI & AD. AD is sometimes informally referred to as “type 3 diabetes” since it’s similar to type 2 diabetes where our bodies have difficulties metabolizing blood sugar, AD patients have difficulty efficiently using energy in their brains which leads to brain cell damage. B3 is believed to help your body convert sugar to energy, and the brain uses over 20% of our body’s energy consumption while only taking up about 2% of our body weight! This is both an opportunity for me to see if a nutritional supplement can give me added clarity without yet another drug in my system, and it’ll help the overall development of solutions for others coming after me with the disease.

I had my first lecanemab infusion! It was a big nothingburger in the end. The nurse at the infusion center was wonderful and walked Jan and I through what to expect in terms of side effects in advance, and we talked through the treatment schedule going forward. She was wonderful and was skilled and gentle with the IV. I was relaxed once the IV was in and had no allergic reaction which would have occurred pretty quickly. The whole process took about 80 minutes. I was vigilant for the next few days watching for potential side effects like headaches, nausea, tiredness, swelling, etc. but I had absolutely none and now I have no anxiety about upcoming infusions. They are a bit inconvenient to have to plan every other Wednesday afternoon to be in the infusion center, but I can live with that … to live!

My long awaited meeting with a new doctor at the Yale University memory disorder clinic finally arrived and I went to meet him the day after my first lecanemab infusion. Compared to the other practice and doctor, this experience was wonderful! As Jan described him, he is like the character Marcus Welby from the old TV show, “Marcus Welby, MD” (only old people would get that). In other words, he was like your dad or grandfather who gives you a big hug and reassures you that everything is alright while giving you badly needed advice based on mountains of experience. As everyone else does, he tested my cognitive capacity and my score on the MoCA test was 29 out of 30 … which is in the normal (or unimpaired) range of 26-30. We talked about my current situation, and he answered every question I asked without judgement or scorn. We even spoke about changing doctors and surprisingly he recommended against it right now. His reasoning was that it would mess up my insurance and could impact my lecanemab treatment schedule. He told me to add him as one of my doctors on all tests and he’d monitor them and give me feedback. He also encouraged me to call him anytime with questions or concerns and we can make an official change when the timing is right so we don’t impact my treatment. How wonderful is that?! Since my insurance authorization ends in April, and my meeting with a third doctor from Mass General Brigham is in March, we can make our decision after the March meeting and work with the insurance company in advance, so we don’t impact my treatments. We talked about my current disease progression and he said we caught this very early, and the new treatments like lecanemab are most effective when started as early as possible so I’m in a good place. He also has high confidence that even better treatments will be coming out in the next year or two which will slow the AD progression even more. We talked about the four pillars of Alzheimer’s prevention – which I have written four separate upcoming articles about – and Jan and I walked away feeling hopeful and much more confident about my future!

So… Wednesday was a successful first infusion, and Thursday was a wonderful meeting with a new doctor, but Friday was the hard day when we told our children and their partners about my diagnosis.

Thankfully those prior two days, as well as the very positive test results I’ve gotten since my initial diagnosis gave us good news to offset the bad. No matter what, it’s hard to tell your children about an incurable, degenerative health diagnosis and my stomach had been in knots since we scheduled the “family video chat.” Having a family video meeting on short notice is always a dead giveaway that something big is about to be announced. Everyone was perceptive enough to know it was probably bad news so they were anxious waiting for the meeting, which was why we scheduled it with very little notice. Derek & Ari and Erica & Doug asked great questions and seemed to take it well (at least on camera). I needed to withhold sharing my diagnosis until we had a full story to tell, but neither Jan nor I liked keeping it from them for so long, and we promised that from that day forward my treatment & prognosis would be an open book that they would get to hear from us first.

The even harder conversation will be with my Mom, Dad and Aunt next weekend. How do you tell your parents and the woman who has been like your second Mom your whole life, that you have an incurable disease like AD?

Keeping this between Jan and myself for 3 months was so incredibly hard, but that very dark place I was in for the first 1-2 months would have been a bad time to share this news with anyone because I wasn’t hopeful at all. I did a ton of research just to write these first 3 months of articles, and that has proven essential for me in understanding where I stand with this damn disease that I’m at war with.

I can now speak from a position of hope and knowledge as I share my story, and it actually feels good to be talking about it openly. It’s very liberating to share, rather than suffering in silence. I wish more people would open up and trust that their support networks will carry them through this rather than abandon them.

Coming Next: The impact of federal funding cuts on critical Alzheimer’s research

Peace my Friends and Thanks for Reading!

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It’s October 31, 2025, and I’m still me. 😊 Happy Halloween!!! I’m going to move to every other week updates now since the learning and progress isn’t coming quite so fast and furiously anymore.

I got a call from my insurance company and they have approved my request to start bi-weekly infusions of the monoclonal antibody drug Leqembi (lecanemab). The approval is for 6 months and then it has to be reapproved. That makes sense because that first 6 months is when a patient will most likely show signs of ARIA if they are going to experience it. ARIA is a dangerous swelling of, and sometimes bleeding in, the brain because of the way this medication passes through the blood-brain barrier (BBB). During that period, the FDA requires multiple MRIs to see if there is any evidence of ARIA. One after the first month, one after the second, one after the third, and one after the sixth. Assuming they are all clear, the insurance will approve continued treatment for another 18 months or more and no further MRIs will be needed to watch for ARIA. Now I’m waiting to hear back from the infusion center about scheduling my first infusion, which I’m a bit anxious about because I dislike needles but tolerate them. I’m also apprehensive because I don’t know the side effects I’ll encounter. Some people are nauseous, some have flu-like symptoms, some have headaches & insomnia.

I had my follow up meeting with my neurologist. Every time I meet with him and his staff, it just reaffirms why I need to find a new team to work with me on this disease! The best way I can describe him is a condescending a$$! My whole professional life I’ve been a technologist that digs into issues and performs research to solve highly technical problems, so right now I’m digging into every solution and research paper I hear about. I had questions for him about real trials going on right now like the GLP-1 (Ozempik) phase 3 trials that will complete this fall which seem to have great promise for dementia as well as its original use for diabetes and follow-on uses for weight loss and cardiac issues. I also asked about comparisons between the two treatments I have available to me right now, lecanemab (Leqembi) and donanemab (Kisunla). They both have different strengths and weaknesses, so I had a novel thought about how to utilize both in a more aggressive and less invasive approach to clearing the amyloid plaque from my brain. His responses were dismissive and insulting to me. He even went as far as to say in a very snotty tone, “you can’t believe everything you read on Reddit.” That really pissed me off and I shot back that my research was done on major medical sites and reputable nationally recognized Alzheimer’s sites. I shut down after that and just wanted to get the heck out of there and hopefully never go back. If a doctor isn’t willing to embrace the inquisitiveness of a patient whom they have diagnosed with an incurable, degenerative disease they should be in a lab, not treating patients. They should be happy that I’m becoming knowledgeable about my disease and encourage thoughtful research.

My neurologist also prescribed an additional medication for me to take alongside the infusions. It’s called Aricept (donepezil) and is an acetylcholinesterase inhibitor. In non-medical gobbledygook that means that it prevents an enzyme (called acetylcholinesterase) from breaking down the neurotransmitter in our brains (called acetylcholine). People with AD have less acetylcholine in our brains and that makes memory and information processing more difficult. It’s not a cure, it just helps with AD symptoms. I have not started taking it, and will wait until I speak with my new neurologist in 2 weeks. I want his opinion first since I don’t believe I have that significant of a cognitive decline to take this with all the potential side effects. My current neurologist wanted to start me on both Aricept and a sleep aid called Belsomra, since Aricept has a side-effect of insomnia. I’m skeptical about the need for these right now, at least in part because I don’t trust him.

On a more positive note, I had my first meeting with one of the studies being conducted by Mass General Brigham Hospital and Harvard Medical School. It’s an 18-month study to track my progress as I receive lecanemab treatments. The first meeting included signing agreements, understanding the study process, and initial memory testing. I’ll be tested for an hour every month through my first 18 months of infusions. It’s a battery of tests that probe into my recall, memorization, summarization of stories, creative storytelling, and strategy. In all the different cognitive tests I’ve been taking, I do well on the story activities and strategy, but less so on the memorization & recall. Afterward they sent me a report on my results and said I should share them with my neurologist. I did that and his medical tech said, “I don’t have any idea what these are, they don’t give me any way to know how you scored.” It’s one more reason why there is no way I’m going to continue to put my life in the hands of this medical group. I had looked up these tests between when they were administered to me and when I went to see my neurologist and they are standard cognitive tests that any expert in this area should be familiar with, yet all they ever do is administer a very simple MoCA (Montreal Cognitive Assessment) test in which I usually get 29 or 30 out of a maximum score of 30, which indicates normal cognitive functioning. It can’t be very hard because even an idiot like Donald Trump says he’s “perfect” when he takes it (though I don’t believe that for a New York minute).

I also had a meeting scheduled with the team from a second AD trial I had signed up for which is a series of 4 hour-long tests in person at Mass General Brigham’s R&D clinic. Each therapy session uses electrical impulses to stimulate your brain into utilizing its energy more effectively, the theory is that results in improving cognition. They administer a cognitive test both before and after to measure any improvement. AD patients typically have low energy levels in their brains which is what creates the brain fog especially in earlier phases of the disease. With starting my infusions and my skin cancer surgery coming up, I decided not to go forward with this program because it requires a drive to Boston every 2 weeks for the 4 tests.

I had dinner with two old friends from my time working at EMC. We’ve been getting together for years periodically, and it had been too long so we met for dinner. We usually got together annually to play golf and honor another good friend and co-worker of ours who lost his battle with brain cancer. It was so good to see them, and we talked about many things that made me feel normal again. We always laugh and joke with each other, and nothing is off limits for busting on one another. Based on that we also laughed and kidded about my news, which while very heavy for them to hear, was new fodder to kid about. That was exactly what I needed, I don’t want my friends to pity me, I want them to understand and accept me for who I am and even laugh with me and my battle. I’m still the same old Scott they’ve known, and will be for a long time to come! Thanks for taking it all in stride and making me feel normal for an evening Mike and Fred!

Though I’m not making my AD diagnosis public yet, I have told a very select group of people I care about when I’m with them in person if we don’t see each other very often. In my mind, good friends deserve to hear this tough news from me live, not through the grapevine. I’m being highly selective right now because I want my family to be among the first to know. I know this is going to be very hard for my family to hear, so I don’t want to share it yet with so many unanswered questions. When I know the full extent of where I stand with the disease’s progression and what my treatment options are, then Jan and I will share the news. They deserve to get a full story, rather than being dragged through the pain of not knowing as Jan and I have been enduring for nearly 3 months now. I still need to get to my first appointment with a doctor that I trust, and that’s the AD expert from Yale I meet with in mid-November, and I also need to get my first lecanemab infusion scheduled. I’m close to finally being able to stop hiding this damn disease from the world.

Coming Next: My 3-Month Update (Telling my family)

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Learning about Alzheimer’s disease (AD) treatments has been harrowing but I’ve had a lot of time to dig in on many sleepless nights early on. Just a few years ago, if someone was diagnosed with AD, there was little that could be done for them aside from make them comfortable with calming drugs.

There are now both “disease modifying” treatments, and symptom abatement medications available for AD, which is a huge step forward in the last few years. Medications can help your brain cope with what’s happening to it, and the newest ones clear the toxins in our brains that kill the brain cells which eventually causes the disease’s progression. None of them are cures, but even having hope of prolonging my cognitive independence is a big step forward!

Note: I am not recommending any of these treatments to you, that is between you and your doctor. I am helping to raise awareness to the treatment options that exist.

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On the day of my diagnosis, my neurologist told Jan and I about 2 different “disease modifying” treatments available by infusion for people like me with minor symptoms. They are lecanemab (Leqembi) and donanemab (Kisunla). Leqembi & Kisunla are the brand names of the drugs, while lecanemab & donanemab are the generic names. While similar, they have some very different features.

Lecanemab was FDA approved in 2023 and donanemab in 2024. They are similar in that they work to prevent amyloid plaque from building up in our brains, but donanemab focuses more on removing existing plaque buildups, while lecanemab focuses on amyloid protein in its early stages before it begins to clump preventing plaque from building up in the first place while slowly clearing the existing deposits. Lecanemab is a bi-weekly infusion, while donanemab is a monthly infusion. Donanemab infusions are stopped after 12-24 months once the plaque levels in the brain are reduced by more than 83%, which is considered “eliminated.” Lecanemab moves to a maintenance mode after 18 months because it continues to prevent plaque buildup from recurring. In July, the FDA also approved a subcutaneous injection form for lecanemab which is far easier than the infusion form, but it’s only used in maintenance mode after an initial 18 months of infusions. So for lecanemab, you have two options for maintenance, a monthly infusion or a weekly self-injection. Since donanemab is newer and does not address the “insoluble” plaque before it clumps in the brain, there is no maintenance mode with it right now but there is talk about how often a person should restart treatments to clear any new buildups.

Based on what I’ve read, donanemab seems to be more effective at rapidly removing existing plaque deposits, while lecanemab is better at preventing future plaque. To me it seems like a hybrid treatment that begins with monthly donanemab infusions to clean up the plaque deposits that could already be damaging our brains, and transitions to lecanemab maintenance treatments to prevent future plaque clumping and its resultant damage would be most effective. It’s also least disruptive on the person being treated. At least from where I stand, used in sequence, they could be a one-two punch: remove first, then protect. Unfortunately, no trials have tested this sequence, and without data, regulators won’t approve it. Since both drugs carry risk of ARIA (see below), combining or sequencing them could amplify that risk. In a climate of National Institute of Health (NIH) budget cuts, launching new trials is harder than ever. However, if long-term data shows that donanemab clears plaques effectively and lecanemab prevents reaccumulation, researchers may propose a sequential trial. What we need is advocacy and storytelling to help shift public and political will toward funding these next-generation studies.

At this point I’ve researched amyloid proteins so much that I think I’ll pull back up to 50,000 feet here and write separate deep dive articles devoted to what amyloid and tau proteins are, and how they go from being a useful part of how our bodies work to being brain cell killers. Watch for those two articles in the future!

Thinking beyond the anti-amyloid treatments, removing all or most of the plaque from my brain doesn’t mean the disease is gone. The cells that were killed by the plaque are still dead, and more will be killed in the future if plaque builds back up. Plus, these treatments don’t directly address tau tangles, which is the other way the disease kills brain cells as it progresses. However, both treatments slow the progression of the disease which is key!

Let’s talk about that for a minute. What does it mean to “slow” the disease’s progression? It means that a person’s scores on clinical progression tests do not decline at the same rate as a typical person with AD. Right now, that slowing of progression is enough to ensure that a person like me will have an extra 6-12 months of cognitive independence before I need to have round the clock care (nursing home or in-home caretakers). That doesn’t sound like very much, especially with the suffocating cost of the treatments, and the inconvenience of infusions. I’m justifying it in my mind right now by thinking that maybe in those extra 12 months something really amazing is discovered to help me.

Here’s the catch, these two treatments have trouble crossing the blood-brain barrier (BBB) so precious little of the drug that is infused actually gets to the places in our brains where it’s needed. I’ve read that a scant 1 in 1,000 units of the drug actually cross the BBB. The act of crossing that BBB can create a risk of ARIA (amyloid related imaging abnormalities). ARIA refers to the changes in the brain seen in MRIs during & after treatment and includes swelling due to the breakdown of the BBB and can cause temporary confusion, headaches and nausea. ARIA can also cause microhemorrhages in the brain – in other words bleeding. These symptoms can either be minor, or serious and cause death. Almost all people with serious ARIA symptoms so far are those that have the APOE e4 homozygote that I discussed in a prior post, and the issue usually occurs in the first six months of treatments.

So people looking to start treatment with lecanemab or donanemab must have a pre-treatment MRI so that their doctors can see how much white matter they’ve lost, and if there is any evidence of brain hemorrhages in the past which would also increase their risk of ARIA in the future during treatment. They also must have a genotyping blood test which will determine whether they carry the APOE e4 variant I discussed in a prior article. The results of both could make them ineligible to have the treatments because the risk of severe ARIA is too great.

If a person is approved for the treatment, they must go through four more MRIs in the first 6 months to see what, if any effect the medication is having, if there are any signs of serious ARIA, and whether doses can be reduced, or must be stopped. With lecanemab, an MRI is required between the second and third doses, another one after four doses, and another one after six doses, and another after 12 doses. I believe the same timeline of 1, 2, 3 and 6 months applies to donanemab as well, but since I’m not receiving donanemab treatments I can’t say for sure.

In the end, I decided to begin treatments with lecanemab. I still wonder at times whether I made the right choice in choosing lecanemab over donanemab, but I’m continuing with the hope that its ability to prevent future buildups with maintenance treatments will benefit me more than rapidly removing the small plaque deposits I already have. In my upcoming deep dive into amyloid protein, I’ll explain more about the donanemab & lecanemab differences and why that impacted my decision. My real hope is banking on much more effective future treatments. Only time will tell.

On the Horizon

There are also some potential new disease modifying treatments in clinical trials. Some are completely new drugs while others are new applications of existing medications, existing vaccines, or over-the-counter supplements.

New Treatments

One exciting new treatment in development is called Trontinemab by Roche. It just began an 18-month phase 3 trial which means it’s likely 2+ years away from FDA approval, but has shown tremendous success with removing amyloid plaque and possibly tau tangles with minimal risk of ARIA. It has solved the blood-brain barrier issue and is far more effective at clearing protein deposits from the brain to an almost imperceptible level at a much more rapid pace! It’s exciting potential, and I need to keep myself in the early stages of AD so I can have a chance at moving to that if/when it’s available. Even if it’s too late for me by then, I’m hopeful for others yet to come. A second trial is in progress for it as a therapeutic treatment for those with an AD predisposition, but no signs of it… like I was 5 years ago.

3/20/26 Update: Another is called remternetug and is being developed by Lilly as a follow-on to Kisunla (donanemab). Remternetug is even more aggressive at clearing plaque, showing that at the highest doses, a patient becomes amyloid-negative at just 3 months! However, the more aggressive a monoclonal antibody treatment is, the more risk it appears to have for an elevated ARIA risk profile as well. It is self-administered at home as an injection which makes it more accessible to people who don’t live near infusion-therapy clinics. Remternetug just completed phase III clinical trials this month. What is still missing are the follow-on reports that show any cognitive benefits, and they are expected to come later this year.

Repurposing Existing Treatments

Believe it or not, a clinical trial completed last year for an erectile disfunction (ED) medication that may fight AD progression. AriBio’s ED medication called AR1001, is being tested as a disease-modifying drug for Alzheimer’s. AR1001 is in Phase 3 trials with ~1,500 participants to see if it could slow early AD progression. The company will share results in the second half of 2026.

The big news last year (2025) was about how GLP-1s (glucagon-like peptide-1) like Ozempik and Wegovy may also slow AD progression. Surprisingly, GLP-1s which were developed for diabetes treatment are showing amazing benefits in other areas too, like weight loss, and to reduce the risk of chronic kidney disease & major cardiovascular events. Today GLP-1s are FDA approved to treat diabetes and weight loss but not AD. However, for the same reasons they are beneficial for diabetes, they were thought to be beneficial for AD.

Sadly, laboratory tests don’t always prove out in human clinical trials. A large clinical trial (EVOKE) for GLP-1s that just finished up in September 2025 did not show a benefit of semaglutide over a placebo in the reduction of AD disease progression, as measured by the change in the Clinical Dementia Rating – Sum of Boxes (CDR-SB) score. While treatment with semaglutide resulted in improvement of Alzheimer’s disease-related biomarkers in both trials, this did not translate into a delay of disease progression. As a result, the 52-week extension of the trial that began in June (EVOKE+) was cancelled. The press release on BioSpace can be found here. I loved Howard Fillit’s take on the failed test because it’s hopeful for where we’ll go in the future!

I’m disappointed that the results of some promising clinical trials didn’t confirm the lab results, but also hopeful that what we learn from this and other trials, whether successful or not, will lead to new treatment approaches in the future.

Here’s a matrix I created to summarize all this info on disease modifying treatments:

Note: A centiloid is a standardized unit used to measure the amount of amyloid plaque in the brain on an amyloid PET scan. The scale ranges from 0 to 100.

0: The average amyloid level in young, amyloid‑negative adults

0-20: Amyloid negative

20-40: Low/early amyloid

40-100: Clearly amyloid-positive

100: Typical for symptomatic Alzheimer’s disease

Beneficial Effects of Vaccines

We find ourselves in a time when proven medical science that saves lives is being systematically attacked with lies and conspiracy theories by our own government. One of those miracles of medicine being attacked is vaccines. Several proven vaccines are showing beneficial side-effects of slowing the diagnosis of and disease progression of Alzheimer’s.

A 2025 study published in Nature tracked more than 250K adults in the UK and found that the shingles vaccine reduced the risk of developing dementia by 20% over a seven-year period. A similar study last year tracking more than 425K adults found that both the shingles & RSV vaccines were associated with reduced dementia risk. More importantly, a follow-up study published in The Washington Post showed that the shingles vaccine may even slow down dementia progression. The vaccine not only reduced the risk of mild cognitive impairment (MCI) for people who were cognitively healthy, but also decreased the mortality rate in people who already had dementia.

Alberto Ascherio, a professor of medicine at Harvard Medical School said, “These findings are promising because they suggest that something can be done. Obviously, the vaccine was not designed or optimized to prevent dementia, so this is sort of an incidental finding. In some ways, we are being lucky.”

I’ll take luck over skill any day if it has impactful results!

The moral of this story is… get your damn shingles vaccine as soon as you are eligible and ignore the moronic war on vaccines by the incompetent Secretary of HHS! I got my two shingles immunizations this past fall. They are painless and I had zero side-effects.

Over-the-Counter Supplements

While people are rejecting proven vaccine science, they are willing to spend literally billions of dollars a year on “nutritional supplements” that often promise miraculous results. Most supplements are ineffective at best, and scams at worse, while doing little or nothing to improve our health. Of the ones that are beneficial, I’ll discuss a few of the more credible brain health related supplements in my coming article on the first pillar of Alzheimer’s prevention, which is diet.

Treating the AD Symptoms

The previous medications are the disease-modifying treatments available or potentially available for people with MCI or mild AD. There are others that deal with symptom abatement, meaning they don’t in any way cure or slow the disease, but they do alleviate some of the debilitating symptoms.

The most commonly prescribed is Aricept (donepezil), which is used to treat AD at all stages. Donepezil can help improve attention, memory, behavior, and the ability to continue daily activities in dementia patients. It’s not a cure for Alzheimer’s disease; it may help improve symptoms, but the disease will continue to progress. Donepezil has been prescribed to me already, but as of publishing this post I have not started taking it. I don’t feel like I have cognitive decline at a level that requires me to take it; and I don’t want to pour drugs into my body that I don’t need, and which won’t slow the progression of the disease.

Namenda (memantine) limits glutamate-cell interactions. Memantine may help slow the decline in memory and thinking skills. It also may play a role in protecting nerve cells. Memantine is approved to treat moderate to severe Alzheimer’s disease. It’s usually taken as a pill or liquid twice a day or as an extended-release pill once a day. Side effects may include dizziness, headache, confusion, hallucinations, agitation and constipation.

The FDA also has approved a combination of those two prior medications, donepezil and memantine, called Namzaric. It’s taken as an extended-release pill once a day. Because more advanced dementia patients struggle to take medications properly, one less pill to track is a good thing.

Belsomra (suvorexant) is used to treat insomnia (trouble sleeping), and not just for dementia patients. It blocks naturally occurring substances in the brain that promote wakefulness called orexins, from making connections in the brain to keep you awake. In turn, this mutes the wakeful effects of orexins and helps you sleep. Deep sleep is when the brain performs cleanup tasks like removing excess tau and amyloid proteins. If you take that a few steps further, those proteins can cause tau tangles & amyloid plaque that kill brain cells. The most common side effect of suvorexant is it can cause you to feel drowsy or less alert the day after you take it.

Rexulti (Brexpiprazole) is an “atypical antipsychotic.” The FDA approved brexpiprazole for treating agitation linked to AD. The medicine is taken as a pill once a day. Warning: Older adults with dementia-related psychosis, such as delusions and hallucinations, who are treated with antipsychotic medicines such as brexpiprazole are at increased risk of death. (kind of makes you wonder why you’d prescribe it in the first place!)

Here’s another table I created to summarize the medications for symptom abatement:

There are likely other medications out there or on the horizon that I haven’t been introduced to yet, and I’ll share them as I learn more … or you can feel free to share what you know in the comments or chat..

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Hopefully this made some sense of the many confusing medications related to AD.

Coming Next: Weeks 9 and 10 Update

Peace my Friends and Thanks for Reading!

Note: What I’m sharing in my deep dive newsletter articles is based on personal research, but please remember I am not in the healthcare profession, and I have no credentials in that area past or present. I’m sharing what I’ve learned, and will continue to learn, in my own desperate effort to advocate for myself when meeting with my care team. I believe everything I share to be correct or I wouldn’t share it, but you should not take anything I say as medical advice.

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It’s October 18, 2025, and I’m still me. 😊 It’s now been 2 months since my AD diagnosis and I’m settling into a new normal. If you didn’t notice, I removed my “trigger warning” beginning this week because I’m feeling that good! It feels like it’s been a transformational week for me. I finally got the results of both my genetic markers test and my skin cancer biopsy. One was good, the other not so much, but it could be a lot worse. I also got out on a solo 3-day backpacking trip this week which was badly needed and cathartic!

Okay so let’s get the bad out of the way first… my biopsy came back as positive for malignant skin cancer on my cheek just below my eye. ☹It’s a basal cell carcinoma and I have to go in for a type of surgery called a “Mohs procedure” next month. It’s not so bad though because it’s outpatient surgery with local anesthetic. How much of my cheek they have to excise will depend on what they find as they remove a layer and inspect it under a microscope. If they find roots extending out of the section of flesh they’ll go back in and take out another layer, and repeat that until there are no cancerous cells left. The good thing is this typer of cancer is 99% curable with the Mohs method and it minimizes the amount of flesh removed in other words; it minimizes the size of the scar. It’s all my fault, I hate the sticky feeling of sunscreen, so I avoid putting it on unless I’m out in the direct sunlight for a prolonged period of time. While Jan always puts it on when out in the sun, I rarely do… but I will now!

If the scar on my cheek is bad, I’ve decided that my story will be that I fought off a raging bear on the trail while backpacking & it got a good swipe in before I drove it off. LOL!

The good news though is my APOE genotyping FINALLY came back from Quest this week. You’ll recall from past posts, people who have a high risk factor for ARIA (brain swelling & bleeding) are not eligible for monoclonal antibody infusions using lecanemab or donanemab. The major risk factor for a person is determined by how many copies of the APOE gene are of the e4 variant (also called an allele). My genotyping came back and both of my APOE alleles are e3 which are not risk factors! Finally, some good news again for me! Once again, I wept tears of relief when I read the results. As a result, the infusion center called me and let me know that they were beginning the final approval process with my insurance company. I had a preliminary approval which hinged on my MRI and genotyping results, so I assume this will be a simple process to get final approval.

Next week I have a follow up with my neurologist and we’ll talk about infusion options and a plan. In November we also have a meeting with an AD expert from Yale University who is the clinical chief of neurodegenerative disorders and specializes in treating patients with cognitive and memory problems. When we meet with him, we’ll validate what we’ve heard and learned so far to make sure I’m on the right path.

Next week I also have meetings with two of the clinical trials being conducted by the REAL Outcomes team at Mass General Brigham. I’ve spoken to both already and they are interested in having me join the studies, now I need to be approved by the doctors leading the work. One of the trials that uses electrical impulses to stimulate brain energy won’t help me long term, but it will help them with research. The other is a study that tracks the efficacy of lecanemab for slowing disease progression and possibly regaining lost cognitive function.

I know it’s a lot, but I will leave no stone unturned to make sure I’m battling this disease in every way available to me!

Compared to all that, it seems anticlimactic, but I also went out for my first solo backpacking trip since my diagnosis. It may not sound like much, but it was a huge confidence builder for me. A diagnosis like this immediately starts tearing down your self-confidence and I need to get back out and restart all the things that are cognitively complex and challenging which are good for my self-confidence, and also good for my brain health! I spent 3 days and 2 nights and hiked 50 miles on the CT blue trail system navigating a complex route I devised to minimize the distance, while also route-finding across a labyrinth of marked and unmarked trails. It felt great to be out there dealing with all the challenges one encounters in the backcountry and proving to myself that I’m still me. Here’s a few pics from the trip, if you want to read about it in detail you can check out the article I wrote last fall in my “Where the Redfern Goes” newsletter. 😊

Coming Next: Alzheimer’s Treatments

Peace my Friends and Thanks for Reading!

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