A Summary of my 15 Most Important Practices for Alzheimer’s Prevention

Knowing my risk, I’m diligent to do everything in my power to avoid a diagnosis of mild cognitive impairment (MCI) or Alzheimer’s. The thought of it is terrifying.
But here’s the truth most people are never told:

The earliest stages are also the most treatable.

Decline is not inevitable. The trajectory can be bent - sometimes dramatically - when the right systems are targeted early and consistently.

One of the most inspiring examples of this is Judy Benjamin, diagnosed with Alzheimer’s 13 years ago, who recently completed a 3,000-mile walk across the United States at age 81 to raise awareness for prevention. Judy is often described as Dale Bredesen’s “Patient Zero,” having implemented his RECODE protocol as outlined in Dr. Bredesen’s book, “The End of Alzheimer’s”.

Judy’s story isn’t a miracle. It’s a roadmap.

Early, aggressive, multi-system intervention can preserve function for years -sometimes more than a decade. And that’s especially true for APOE4 carriers.

Why Early Intervention Matters

Alzheimer’s doesn’t begin with memory loss. It begins silently, years earlier, with:

• Glucose hypometabolism

• Mitochondrial dysfunction

• Synapse loss

• Chronic neuroinflammation

• Sleep disruption

• Lipid and membrane breakdown

The earlier you interrupt these cascades, the more brain you preserve.

My 15 Most Important Staples for Early Alzheimer’s Prevention

I’m not waiting for a diagnosis. I’ve been implementing extensive prevention strategies in my daily life since finding out my APOE4/4 status years ago.

These are the interventions with the strongest human data, the most compelling biology, and the best real-world results, particularly for APOE4 carriers.

1. Fix Metabolism, Insulin Resistance, and Gut Health (the #1 lever)

Brain energy failure appears years before symptoms.

Targets:

• Fasting glucose: 75–85 mg/dL

• A1C: ≤ 5.2

• Fasting insulin: < 4

• Microbiome testing and correction

Metabolic repair stabilizes cognition better than almost any drug.

2. High-Dose DHA (2–3 g/day, APOE4-aware) and PC

APOE4 brains struggle to transport DHA across the blood–brain barrier.

High-DHA intake (especially DHA-PC) supports:

• Synapse repair

• Reduced neuroinflammation

• Slower hippocampal atrophy

PC supports:

• Synaptic membranes

• DHA delivery

• Neurotransmission

• Lipid balance

PC + DHA is one of the most effective synaptic repair combinations. I eat SMASH fish (Sardines, Mackerel, Anchovies, Salmon, Herring) at least 4 times a week, which is a more effective delivery of phospholipid DHA to the brain than taking a supplement! (I skip the anchovies because I don’t like their salty taste).

3. Plasmalogens (Neuro + Glia)

Plasmalogens drop early in Alzheimer’s. Supplementation has been shown to:

• Improve memory

• Increase cognitive scores

• Support synaptic integrity

I’ve used plasmalogens for years. They aren’t cheap - but neither is cognitive decline. Studies show that those with the highest brain plasmalogens have the lowest incidence of dementia.

4. Lower Homocysteine (< 7 µmol/L)

High homocysteine predicts brain atrophy and faster decline - yet is rarely tested.

Lowering it slows progression in randomized trials.

Key tools:

• Methyl or hydroxy-B12 (injections early on)

• Methylated folate

• TMG (trimethylglycine)

Nearly half the population carries an MTHFR gene variant and doesn’t know it. It can negatively impact methylation - a vital process for DNA, neurotransmitters and detoxification.

5. Repair Sleep Architecture (Critical for APOE4)

Sleep is when the brain clears amyloid and tau.

Foundational supports:

• Melatonin (≥ 2–3 mg; I personally use higher doses)

• Glycine, magnesium, L-theanine

• Evening red light

• Consistent bedtime

• Eliminate alcohol - it obliterates deep sleep!

6. Reduce Neuroinflammation (Microglial Control)

Chronic inflammation accelerates decline.

Helpful tools include:

• DHA

• Curcumin

• Optimized vitamin D

• Polyphenols

• Melatonin

• Low-dose aspirin (if appropriate)

• Low-dose naltrexone (LDN) to reduce hs-CRP … this addition to my stack made a marked improvement in my hs-CRP - now usually below 0.5!

7. Mild Ketosis (APOE4-Friendly)

Ketones bypass glucose failure and fuel neurons directly.

My Goal: mild, not extreme ketosis

• Low-glycemic diet

• 12–14 hour overnight fast

• C8 MCT powder (better lipid profile for APOE4). While I am not on a ketogenic diet due to my slender build and having no weight to lose, I add C8 MCT Powder to my morning coffee and I am generally in mild ketosis in the hours before noon. (0.5 – 2 mmol/L)

8. Lithium (Low-Dose, Neuroprotective)

Lithium is one of the most underappreciated neuroprotective tools available.

Low-dose lithium:

• Inhibits GSK-3β (tau phosphorylation)

• Enhances autophagy

• Supports mitochondrial resilience

• Is associated with lower dementia rates in epidemiologic studies

This is not psychiatric-dose lithium and generally has no noticeable side effects.

9. NAD⁺ Support (Cellular Energy & Repair)

NAD⁺ declines with age and is critical for:

• Mitochondrial function

• DNA repair

• Sirtuin activation

• Neuronal survival

Support options include:

• NMN or NR

• NAD⁺ injections or infusions (advanced)

• Exercise and fasting (foundational)

Energy failure is an early Alzheimer’s event - NAD directly addresses it.

10. Daily Exercise — Non-Negotiable

Exercise raises BDNF and slows progression.

AD-optimized formula:

• Zone 2: 45 min, 5–6×/week

• Strength training: 3×/week

• Steps: 10,000–12,000/day

I do 20 minutes of weight training every other day. Usually two sets (12 repetitions) of 5-6 exercises. Minimum 3 times a week I add a 45 minute Nordic Walking hike through a peaceful woodland preserve in my neighborhood. In addition, I use my rebounder daily, usually enjoying two 15 minute sessions of jumping to my favorite music!

11. Thyroid Optimization (Especially T3)

Low thyroid function - especially low T3 - accelerates decline.

Targets:

• Free T3: upper third of range

• Reverse T3: low. (I’ve fine-tuned mine to <11)

Cellular hypothyroidism = cognitive vulnerability. If you’re on Levothyroxine replacement therapy, please check out my previous post on the topic!

12. Red / Near-Infrared Light (Photobiomodulation)

Supports:

• Mitochondrial ATP

• Cerebral blood flow

• Neuronal repair

• Sleep quality

• Reduced inflammation

Often used alongside metabolic and exercise therapy in long-term success cases. I use redlight therapy daily and believe it’s a non-negotiable addition to brain protection.

13. Melatonin (Neuroprotective Doses)

Melatonin:

• Reduces oxidative stress

• Stabilizes mitochondria

• Modulates protein phase separation

• Reduces tau and amyloid toxicity

For APOE4 carriers, melatonin is profoundly protective.

14. HBOT (Hyperbaric Oxygen Therapy)

HBOT is one of the most promising non-pharmacologic interventions for early cognitive decline.

Emerging human data show improvements in:

• Cerebral blood flow

• Mitochondrial function

• Processing speed and memory

• Neuroinflammation

• Sleep and overall energy

By increasing dissolved oxygen in plasma, HBOT enhances mitochondrial ATP production, supports angiogenesis, and improves tissue repair - all critical in a brain suffering from hypometabolism.

If accessible, HBOT is a high-leverage investment early in the disease process.
I personally invested in my own chamber in 2025 and noticed meaningful improvements in energy, drive, and overall well-being within the first few weeks.

15. Rapamycin (Intermittent, Carefully Dosed)

Rapamycin targets one of the core drivers of neurodegeneration: chronic mTOR overactivation.

When used intermittently and at low doses, rapamycin may:

• Enhance autophagy (clear damaged proteins and organelles)

• Reduce neuroinflammation

• Improve mitochondrial efficiency

• Support vascular and immune health

Importantly, this is not daily immunosuppression. In longevity and neuroprotection contexts, rapamycin is pulsed, with careful attention to dose, timing, and individual response.

I’ve been taking once weekly rapamycin since 2021. With occasional breaks to wash out any residual buildup, I believe it’s an easy strategy for anyone past reproductive years carrying the APOE4 gene to protect the blood-brain barrier integrity.

The Takeaway

You cannot “cure” Alzheimer’s - but you can implement a thoughtful prevention strategy and, especially when addressed early, potentially change its trajectory. Dale Bredesen’s books The End of Alzheimer's and The End of Alzheimer's Program offer an invaluable roadmap for anyone concerned about Alzheimer’s disease - whether for themselves or a loved one.

Judy Benjamin’s 3,000-mile walk sends a clear message to everyone:

You are not powerless.
Your brain is not doomed.
Your choices matter.

Disclaimer

This article reflects my personal research, experience, and health practices and is shared for educational and informational purposes only. It is not medical advice and should not be used to diagnose, treat, or replace guidance from a qualified healthcare professional.

Many of the interventions discussed - including supplements, peptides, off-label medications, hyperbaric oxygen therapy, and lifestyle strategies - may not be appropriate for everyone and can carry risks depending on individual health status, genetics, and medications. Decisions about medical treatment should always be made in consultation with a knowledgeable physician.

Alzheimer’s disease and cognitive decline are complex, multifactorial conditions. While early, multi-system intervention may improve outcomes or slow progression, no intervention discussed here is presented as a cure.

If you are new here: APOE status is determined primarily by two SNPs (genetic markers): rs429358 and rs7412. In most direct-to-consumer genetic reports, APOE4/4 corresponds to rs429358 C/C and rs7412 C/C.