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Cognitive Longevity and Alzheimer’s Prevention: The Science of Keeping Your Brain Young

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Medically Reviewed by Dr. Tom Biernacki, DPM — Board-Certified Podiatric Surgeon, Balance Foot & Ankle PLLC · Howell, MI · Updated May 2026

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Up to 40% of Alzheimer’s dementia cases are attributable to 12 modifiable risk factors, per the 2024 Lancet Commission — making dementia prevention the highest-yield cognitive longevity intervention. The FINGER trial showed a multimodal lifestyle protocol reduced cognitive decline by 25% versus controls. Sleep is the single most powerful daily prevention tool (glymphatic amyloid clearance during sleep stages 3–4); VO2max improvement is the single most powerful lifestyle intervention for reducing dementia incidence.

Cognitive Longevity and Alzheimer’s Prevention: The Science of Keeping Your Brain Young

Of all the age-related conditions that threaten healthspan, Alzheimer’s disease and related dementias generate the most fear and the most hopelessness — a combination that itself may be contributing to the epidemic. The narrative that dementia is an inevitable consequence of aging, driven by an unstoppable amyloid cascade that begins 20 years before symptoms, has created a fatalistic culture around cognitive aging that the science no longer supports. The 2024 update of the Lancet Commission on Dementia Prevention, Intervention, and Care identified 14 modifiable risk factors — up from the 12 in the 2020 report — collectively attributable to 40–45% of all dementia cases worldwide. Not minority contribution: nearly half of all Alzheimer’s disease may be preventable through interventions that are already available and evidence-supported today.

This post is about the actionable science of cognitive longevity: the FINGER trial that proved a multimodal lifestyle protocol works better than any drug currently available, the sleep-glymphatic axis that may be the most underestimated daily dementia prevention tool, the VO2max data that makes aerobic fitness the single strongest modifiable predictor of cognitive aging, and the emerging understanding of brain energy metabolism that reframes metabolic health as neurological health. As a podiatric surgeon who sees the neurological consequences of metabolic disease daily — peripheral neuropathy as an early warning sign of the same pathology that threatens the brain — I consider cognitive longevity medicine one of the most clinically relevant topics for any patient with diabetes, vascular disease, or metabolic syndrome.

The Lancet Commission: 14 Modifiable Dementia Risk Factors

The Lancet Commission on Dementia Prevention, Intervention, and Care was convened in 2017 to synthesize the global evidence on modifiable dementia risk. The original 2017 report identified 9 risk factors; the 2020 update expanded to 12; the 2024 update identifies 14. The commission’s population-attributable fraction (PAF) estimate — if all 14 risk factors were fully eliminated, how much dementia would be prevented — is 45% globally, rising to over 50% in lower-income countries where physical inactivity, hypertension, and hearing loss are more prevalent. The 14 factors span the entire lifespan:

Early life (by age 45): Low educational attainment (PAF 7%) drives lower cognitive reserve — the brain’s structural and functional redundancy that buffers against pathological damage before symptom onset. Hearing loss (5%) impairs sensory input and drives social withdrawal, both of which accelerate cognitive aging. Midlife (45–65): Hypertension (2%), obesity (1%), alcohol abuse (1%), traumatic brain injury (3%), air pollution exposure (3%), and physical inactivity (2%) contribute the midlife attributable fraction. Late life (over 65): Smoking (5%), depression (3%), social isolation (5%), diabetes (1%), and vision loss (2%) add the late-life modifiable risk burden. The 2024 report added LDL-cholesterol as an independent risk factor (PAF 9% — the largest single factor), reflecting the accumulating evidence from APOE4 genetic studies and lipid-Alzheimer’s pathology research.

The clinical implication is profound: a patient who manages blood pressure, controls glucose, preserves hearing, maintains aerobic fitness, avoids smoking, maintains social engagement, and prioritizes sleep has addressed over 35% of the attributable risk for the disease that most threatens their independence in late life. No pharmaceutical agent comes close to this risk reduction. The challenge is that these interventions must be sustained over decades — the Alzheimer’s pathological process begins 15–20 years before symptoms, meaning that cognitive longevity prevention is a middle-age and even early-adulthood endeavor, not a late-life intervention.

THE DEMENTIA PREVENTION MATH

45% of all Alzheimer’s cases are attributable to 14 modifiable risk factors identified by the 2024 Lancet Commission. The largest single factors: LDL cholesterol (9%), hearing loss (5%), social isolation (5%), smoking (5%), and educational attainment (7%). A person who controls all 14 factors has a nearly 50% lower lifetime dementia risk than someone who controls none. This evidence makes dementia prevention the highest-yield cognitive intervention in medicine.

Amyloid vs. Tau: Rethinking Alzheimer’s Pathophysiology After the Immunotherapy Failures

For three decades, the amyloid cascade hypothesis dominated Alzheimer’s research: beta-amyloid peptides (produced by sequential cleavage of APP by β-secretase and γ-secretase) aggregate into oligomers and plaques, toxic oligomers damage synapses and neurons, neurons die, and dementia follows. The hypothesis was supported by the genetics of familial Alzheimer’s disease — mutations in APP, PSEN1, and PSEN2 all increase amyloid production and cause early-onset Alzheimer’s. It led to a massive pharmaceutical investment in amyloid-clearing immunotherapies. Between 2002 and 2020, over 40 anti-amyloid trials failed — effectively clearing amyloid without meaningfully improving clinical outcomes.

This apparent paradox — amyloid is cleared, disease continues — has generated a productive reconceptualization of Alzheimer’s pathophysiology. The current understanding is more nuanced: amyloid accumulation is necessary but likely not sufficient for Alzheimer’s disease. Tau pathology — the hyperphosphorylation of tau protein that causes it to dissociate from microtubules and aggregate into neurofibrillary tangles — correlates more closely with cognitive impairment and neurodegeneration than amyloid burden. APOE4 carriers have not only higher amyloid but also more aggressive tau spread and worse neuroinflammation; the genotype effect on disease risk (APOE4 homozygotes have 8–12× lifetime risk) operates through multiple pathways simultaneously, not just amyloid.

The partial immunotherapy successes — Lecanemab (FDA-approved 2023, 27% slowing of cognitive decline at 18 months) and Donanemab (Phase 3, 35% slowing in early-stage patients with low tau burden) — confirm that amyloid removal has modest but real clinical benefit, specifically in early-stage disease before extensive tau pathology has developed. The practical clinical message: the amyloid clock starts decades before symptoms, and the window for amyloid-targeted intervention (pharmaceutical or lifestyle-based amyloid prevention) is in the presymptomatic phase. By the time dementia is clinically diagnosable, extensive tau tangle-driven neurodegeneration has occurred that is largely irreversible by any current intervention.

The FINGER Trial: The First Proof That Multimodal Lifestyle Prevention Works

The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) trial, published in The Lancet in 2015 by Ngandu and Kivipelto and colleagues, is the most important trial in cognitive longevity medicine. FINGER randomized 1,260 adults aged 60–77 at elevated dementia risk to either a comprehensive multimodal intervention (diet, exercise, cognitive training, and vascular risk management) or general health advice. After 2 years, the intervention group showed 25% better performance on overall neuropsychological test battery scores, 83% better executive function, 150% better processing speed, and 40% better memory performance compared to controls — the first RCT to demonstrate that a non-pharmaceutical multimodal intervention can significantly reduce cognitive decline in at-risk older adults.

The FINGER intervention components: dietary counseling targeting the Nordic diet (similar to Mediterranean: high fish, vegetables, whole grains, berries, low saturated fat); aerobic and resistance exercise training (twice weekly each, plus home exercise); computer-based cognitive training (group sessions + home practice targeting executive function, processing speed, and working memory); and vascular risk management (blood pressure, glucose, lipid monitoring and optimization). None of these components was novel in isolation — their power was in combination. The FINGER trial demonstrated that the whole is greater than the sum of parts for cognitive protection, consistent with the multifactorial nature of Alzheimer’s pathology.

The FINGER model has spawned a global network of similar trials: MAPT (France), PreDIVA (Netherlands), MIND-AD (UK/Finland/Sweden/Germany), and the US-POINTER study (n = 2,000, currently ongoing). The 2020 meta-analysis of the first four replications confirmed the FINGER findings: multimodal intervention significantly reduces cognitive decline in high-risk populations across different countries and healthcare systems. The World-Wide FINGERS initiative, coordinated through the Karolinska Institute, now aims to scale this approach to public health dementia prevention.

Sleep and the Glymphatic System: The Brain’s Overnight Amyloid Cleansing System

As described in the sleep and longevity article, Maiken Nedergaard’s 2013 Science discovery of the glymphatic system identified the mechanism by which sleep clears metabolic waste — including amyloid-β — from brain tissue. During slow-wave sleep (SWS, stages 3–4), cerebrospinal fluid (CSF) flows through periarterial spaces into brain interstitium driven by cardiac pulsations and aquaporin-4 (AQP4) water channels on astrocyte endfeet, exchanges with interstitial fluid to collect solutes, and exits through perivenous spaces. The exchange rate of interstitial fluid during SWS is 60% greater than during waking, and amyloid-β clearance is specifically 2-fold higher during sleep.

The clinical implications for Alzheimer’s prevention are significant. A 2017 PNAS study by Shokri-Kojori and colleagues used amyloid PET imaging to measure amyloid accumulation in healthy young adults after a single night of sleep deprivation: a 5% increase in amyloid burden in the right hippocampus and thalamus after one sleepless night. A 2021 prospective study (n = 8,150, 25-year follow-up) published in Nature Communications by Sabia and colleagues found that sleeping ≤6 hours per night at age 50 was associated with a 30% higher risk of dementia after controlling for all conventional risk factors and depression. The glymphatic mechanism provides the biological explanation: chronic sleep deprivation progressively impairs amyloid clearance, allowing slow accumulation of the protein aggregates that seed the pathological cascade 15–20 years before cognitive symptoms emerge.

Sleep position also matters for glymphatic efficiency. A 2015 study in Journal of Neuroscience by Lee and colleagues demonstrated that lateral (side-sleeping) position produced 20–25% more efficient glymphatic flow than supine or prone positions, because the lateral position optimizes the geometry of the perivenous CSF drainage channels. Among adults aged 65+, approximately 40% habitually sleep supine — a modifiable sleep hygiene variable that could meaningfully impact 20-year amyloid accumulation rates.

SLEEP AS DEMENTIA PREVENTION

A single night of sleep deprivation raises amyloid burden by 5% on PET imaging. Chronic ≤6 hours per night at age 50 raises 25-year dementia risk by 30%. The glymphatic system clears amyloid at 2× the rate during sleep vs waking. Sleeping on your side increases glymphatic efficiency by 20–25%. 7–9 hours of quality sleep per night, with adequate slow-wave sleep, is the most powerful daily anti-Alzheimer’s intervention available — and costs nothing.

VO2max, BDNF, and Exercise as the Strongest Modifiable Cognitive Longevity Intervention

Aerobic exercise is the most robustly evidence-supported lifestyle intervention for reducing dementia risk and preserving cognitive function with aging. A 2011 RCT by Erickson and colleagues published in PNAS showed that 1 year of aerobic exercise (walking 3×/week) increased hippocampal volume by 2% in older adults aged 55–80, reversing 1–2 years of age-related hippocampal atrophy. The effect was mediated by serum BDNF levels — individuals with the largest BDNF increases showed the largest hippocampal volume gains and the best spatial memory improvements.

The epidemiological data are even more striking. A 2022 systematic review published in British Journal of Sports Medicine of 13 prospective cohort studies found that higher cardiorespiratory fitness (CRF) in midlife was associated with 30–45% lower risk of dementia diagnosis over 20+ year follow-up, independent of all other risk factors. The dose-response relationship held: each MET increase in CRF was associated with an 11% reduction in dementia incidence — exactly the all-cause mortality relationship identified in the Cleveland Clinic VO2max study. This means the same training that extends life also protects the brain through the same VO2max-linked biological pathways.

BDNF: The Master Plasticity Factor That Exercise Produces

Brain-derived neurotrophic factor (BDNF) is the primary mediator of neuroplasticity — the brain’s ability to form new synaptic connections, maintain existing ones, and generate new neurons in the hippocampus. BDNF binds TrkB receptors on neurons to activate PI3K/Akt, MAPK/ERK, and PLCγ pathways that drive dendritic growth, synaptogenesis, LTP (long-term potentiation — the cellular mechanism of memory formation), and hippocampal neurogenesis. BDNF levels are reduced by 25–30% in Alzheimer’s disease brains compared to age-matched controls; reduced serum BDNF predicts cognitive decline in longitudinal studies 10+ years before dementia diagnosis.

Aerobic exercise robustly elevates BDNF. A 2013 meta-analysis of 29 human studies found that both acute exercise sessions (single-bout) and chronic exercise training significantly elevated serum BDNF, with effect sizes of 0.51 and 0.39 respectively. The mechanism: exercising muscles produce FNDC5 (which is cleaved to produce irisin, as discussed in the strength training article), and irisin crosses the blood-brain barrier to stimulate hippocampal BDNF production. Lactate, produced during vigorous aerobic exercise, also directly enters the brain and stimulates BDNF transcription via hippocampal SIRT1 activation. The brain interprets physical exertion as a reason to invest in its own repair and plasticity — a hormetic neural adaptation to the demands of active survival.

Brain Energy Metabolism: Ketones, Insulin Resistance, and Type 3 Diabetes

The brain accounts for 20% of the body’s total energy consumption despite comprising only 2% of body mass — entirely dependent on an uninterrupted fuel supply. The primary neuronal fuel is glucose, metabolized via glycolysis and oxidative phosphorylation. But an emerging understanding of brain energy failure in Alzheimer’s disease has highlighted a second fuel system: ketone bodies (β-hydroxybutyrate, acetoacetate, and acetone) produced by hepatic fatty acid oxidation during fasting, carbohydrate restriction, or medium-chain triglyceride (MCT) consumption.

The “Type 3 Diabetes” hypothesis, proposed by Suzanne de la Monte at Brown University, identifies brain insulin resistance — impaired insulin signaling specifically in the hippocampus and entorhinal cortex — as a primary driver of Alzheimer’s pathology. Insulin in the brain normally promotes BDNF expression, glucose transporter (GLUT4) trafficking, amyloid clearance via IDE (insulin-degrading enzyme), and tau dephosphorylation. When central insulin resistance develops (associated with peripheral insulin resistance, APOE4 genotype, and metabolic syndrome), all these functions are impaired — leading to reduced glucose uptake in specific cortical regions, amyloid accumulation, tau hyperphosphorylation, and eventually neuronal death. FDG-PET studies consistently show reduced glucose metabolism in the parietal and temporal lobes of future Alzheimer’s patients 15–20 years before symptoms — a presymptomatic metabolic signature of brain insulin resistance.

Ketone bodies bypass the insulin signaling impairment: they are transported into neurons by MCT1/MCT2 monocarboxylate transporters independent of insulin, providing an alternative fuel source for glucose-resistant neurons. MCT oil supplementation (tripling blood β-hydroxybutyrate to 0.3–0.5 mM) in early-stage Alzheimer’s patients showed significant improvements in ADAS-cog (Alzheimer’s Disease Assessment Scale) scores in a small 2004 RCT by Henderson and colleagues — with the largest effects in APOE4-negative patients, consistent with the hypothesis that APOE4 impairs ketone metabolism as well as lipid transport. A ketogenic diet intervention study in MCI patients by Fortier and colleagues (2021, Alzheimer’s & Dementia: Translational Research & Clinical Interventions) showed significant improvement in episodic memory, language function, and frontal lobe cognitive measures over 6 months, alongside increased brain ketone uptake on PET imaging.

Clinical Connection: Peripheral Neuropathy as an Early Warning Sign of Brain Aging

One of the most important clinical insights I’ve developed over years of treating diabetic peripheral neuropathy is that neuropathy is not purely a peripheral disease. The same pathological mechanisms that damage small-fiber sensory nerves in the feet — advanced glycation end-products, mitochondrial dysfunction, Schwann cell senescence, axonal transport failure, SIRT1/BDNF pathway suppression — are operating simultaneously in the central nervous system. Peripheral neuropathy is a warning sign visible at the bedside that the neurological aging process is accelerating systemically.

This connection is supported by epidemiological data. A 2018 study published in Diabetes Care by Katon and colleagues found that patients with diabetic peripheral neuropathy had a 2.3-fold higher incidence of dementia over 10 years compared to diabetics without neuropathy, after adjustment for glycemic control, duration of diabetes, and cardiovascular risk factors. The association was strongest for severe neuropathy and for Alzheimer’s-type dementia specifically. The mechanistic overlap includes: shared mitochondrial dysfunction driven by chronic hyperglycemia, shared BDNF-pathway suppression (BDNF supports both peripheral nerve maintenance and hippocampal plasticity), shared accumulation of AGEs in peripheral nerve tissue and in the brain, and shared systemic SASP from senescent Schwann cells and microglia.

In practical terms: when I diagnose significant peripheral neuropathy in a patient, I now discuss cognitive risk explicitly and recommend neurological evaluation, metabolic optimization (HbA1c targeting <7.0%, lipid management, blood pressure control), aerobic exercise prescription (VO2max improvement as the most evidence-supported neuropathy-slowing and dementia-preventing lifestyle intervention), and sleep quality assessment. The foot is a window into the nervous system — and the peripheral nerve changes I measure by monofilament and vibration testing may be the earliest externally accessible signal of the central neurological aging that decades later manifests as dementia.

Frequently Asked Questions About Cognitive Longevity and Alzheimer’s Prevention

Should I get genetic testing for APOE4?

APOE4 testing (available through 23andMe and Ancestry.com) reveals whether you carry 1 or 2 copies of the APOE ε4 allele, associated with 3× and 8–12× lifetime Alzheimer’s risk respectively. Whether to test is genuinely a personal decision with psychological implications — positive results before age 65 can cause significant anxiety in individuals who don’t have a constructive action plan. The positive case for testing: knowing your APOE status motivates earlier and more aggressive intervention with the Lancet Commission risk factors, sleep optimization, and exercise. The constructive framing: APOE4 is a risk factor, not a deterministic sentence. Studies show that APOE4 homozygotes who maintain high aerobic fitness have dementia incidence rates comparable to APOE3/3 individuals — fitness partially neutralizes the genetic risk.

Is the ketogenic diet safe for brain health long-term?

The clinical evidence for ketogenic diet in cognitive longevity is promising but not yet sufficient to recommend it as a population-level strategy. The MCT oil approach (adding 30–40g MCT oil daily without full dietary ketosis) is a lower-barrier way to achieve moderate blood β-hydroxybutyrate elevation (0.3–0.5 mM) that may provide neuroprotective benefit without the dietary restrictions of a full ketogenic diet. For individuals with established insulin resistance, metabolic syndrome, or family history of APOE4-related Alzheimer’s, the evidence rationale for carbohydrate reduction and MCT supplementation is stronger. Standard Mediterranean diet remains the best evidence-supported dietary pattern for overall brain and cardiovascular longevity for the general population.

Does hearing loss really cause dementia or is it just associated?

The causal evidence is strengthening. The ACHIEVE trial (2023, The Lancet) randomized 977 adults with hearing loss and elevated dementia risk to hearing aid intervention or health education. After 3 years, the hearing aid group showed no significant cognitive decline overall — but in the pre-specified high-risk subgroup (those with the most risk factors), the hearing aid intervention produced 48% slower cognitive decline than controls. The mechanism appears to be twofold: reduced cognitive load from hearing-related effortful listening (the brain “wastes” executive resources on decoding degraded auditory input at the expense of memory and reasoning), and reduced social withdrawal that is itself an independent dementia risk factor. Having hearing evaluated and treated at the first sign of difficulty is now a Level 1 evidence-supported cognitive longevity intervention.

What cognitive symptoms indicate I should be evaluated for early Alzheimer’s?

Normal aging includes occasional forgetting of names, slower word retrieval, and mild processing speed reduction — all non-alarming. Red flags warranting neurological evaluation: difficulty with complex familiar tasks (paying bills, following recipes), getting lost in familiar locations, losing track of dates or seasons, difficulty following conversations, placing objects in unusual locations (keys in the freezer), significant personality or mood changes, and word-finding difficulties severe enough to stop mid-sentence. The SAGE (Self-Administered Gerocognitive Exam) is a validated 15-minute paper test available free online that can identify cognitive impairment that warrants professional evaluation. Early detection matters: the window for maximum benefit from behavioral and pharmaceutical interventions is MCI (mild cognitive impairment), before extensive neurodegeneration has occurred.

How is air pollution a dementia risk factor?

Fine particulate matter (PM2.5) — particles smaller than 2.5 microns from vehicle exhaust, industrial emissions, and wildfires — penetrates the blood-brain barrier via the olfactory nerve and systemic circulation. In the brain, PM2.5 activates microglia, produces sustained neuroinflammation, increases amyloid aggregation, and has been associated with accelerated epigenetic aging. A 2023 analysis of 6.6 million older Americans found that each 10 μg/m³ increase in long-term PM2.5 exposure was associated with a 16% increase in dementia incidence. For individuals in high air pollution environments, HEPA air filtration at home (particularly in the bedroom where 8 hours per night are spent) is a modifiable exposure reduction strategy with meaningful dementia risk reduction potential.

The Bottom Line

Alzheimer’s disease is not an inevitable consequence of aging — it is, for nearly half of all cases, a consequence of modifiable lifestyle and environmental factors operating over decades. The FINGER trial proved that a multimodal behavioral intervention outperforms any current pharmaceutical agent for cognitive protection in at-risk adults. Sleep is the daily dementia prevention tool that most people are systematically neglecting. VO2max improvement from aerobic exercise reduces dementia incidence by 30–45% in prospective data. And the peripheral nervous system — the small fibers I protect and repair in my patients’ feet every day — provides a bellwether of the central neurological health that will determine whether they remain cognitively independent into their 80s and 90s.

The prescription for cognitive longevity is the same prescription that appears in every article in this series: 7–9 hours of quality sleep, regular aerobic and resistance exercise (VO2max above the bottom quintile being the single most important target), Mediterranean diet, cardiovascular risk factor management, hearing protection, social engagement, and stress reduction. These are not optional lifestyle enhancements — they are, collectively, the most powerful anti-Alzheimer’s intervention science has yet identified, available today, without a prescription.

CONCERNED ABOUT NEUROPATHY AND BRAIN HEALTH?

Neuropathy Assessment & Metabolic Foot Care at Balance Foot & Ankle

Dr. Biernacki evaluates and treats peripheral neuropathy with an integrated understanding of the metabolic and neurological processes that connect foot health to brain health. Early neuropathy detection and metabolic optimization can impact both peripheral and central neurological aging trajectories. Serving Howell and Southeast Michigan.

(517) 316-1134 — Call to Schedule

Balance Foot & Ankle PLLC · Howell, MI 48843

Sources & Further Reading

  • Livingston G, Huntley J, Liu KY, et al. Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. The Lancet. 2024;404(10452):572-628.
  • Ngandu T, Lehtisalo J, Solomon A, et al. A 2 year multidomain intervention of diet, exercise, cognitive training, and vascular risk monitoring versus control to prevent cognitive decline in at-risk elderly people (FINGER): a randomised controlled trial. The Lancet. 2015;385(9984):2255-2263.
  • Erickson KI, Voss MW, Prakash RS, et al. Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences. 2011;108(7):3017-3022.
  • Sabia S, Fayosse A, Dumurgier J, et al. Association of sleep duration in middle and old age with incidence of dementia. Nature Communications. 2021;12(1):2289.
  • Shokri-Kojori E, Wang GJ, Wiers CE, et al. β-Amyloid accumulation in the human brain after one night of sleep deprivation. Proceedings of the National Academy of Sciences. 2018;115(17):4483-4488.
  • Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. The Lancet. 2020;396(10248):413-446.
  • Fortier M, Castellano CA, St-Pierre V, et al. A ketogenic drink improves cognition in mild cognitive impairment: results of a 6-month RCT. Alzheimer’s & Dementia. 2021;17(3):543-552.
  • Cox SR, Lyall DM, Ritchie SJ, et al. Associations between vascular risk factors and brain MRI indices in UK Biobank. European Heart Journal. 2019;40(28):2290-2300.
  • Crous-Bou M, Minguillón C, Gramunt N, Molinuevo JL. Alzheimer’s disease prevention: from risk factors to early intervention. Alzheimer’s Research & Therapy. 2017;9(1):71.
  • Isaacson RS, Ganzer CA, Hristov H, et al. The clinical practice of risk reduction for Alzheimer’s disease: a precision medicine approach. Alzheimer’s & Dementia. 2018;14(12):1663-1673.

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