Alzheimer's Disease & Other Dementias

Progressive neurodegeneration marked by amyloid plaques and tau tangles.1 Several modifiable risk factors are linked with dementia risk, and a multidomain lifestyle program has shown a modest benefit; no supplement has been shown to prevent it.2

Neurological & Mental Health Evidence-Based

Last updated:

What Is Alzheimer's Disease?

Alzheimer's disease is the most common form of dementia (contributing to 60 to 70% of cases3), characterized by progressive cognitive decline, memory loss and behavioral changes. It is defined pathologically by amyloid-beta plaques and tau neurofibrillary tangles, with widespread neuron loss particularly in the hippocampus and cortex.

It is increasingly understood as multifactorial, with vascular factors, inflammation and metabolic health all studied as contributors; brain insulin resistance is one hypothesis under investigation. A structured assessment looks for reversible contributors such as depression, thyroid disease, B12 deficiency, sleep apnea and sedating medicines.

Critical insight: pathology begins 15 to 20 years before symptoms1. The window for prevention is now, in middle age. Lifestyle measures such as diet, exercise, sleep, social engagement and cognitive activity are linked with lower risk, and the FINGER trial found a modest cognitive benefit from combining them.

๐Ÿ’ก Key Insight: ~45% of dementia cases are attributable to 14 modifiable risk factors (Lancet Commission 2024)4: hearing loss, LDL cholesterol, depression, head injury, hypertension, smoking, obesity, diabetes, alcohol, physical inactivity, social isolation, air pollution, vision loss, low education. The figure is a population estimate; evidence that tackling these factors lowers risk is stronger than it was4.
A side view of a brain with small brown spots, above two nerve cells: a healthy neuron with long smooth branches, and an affected neuron with shorter broken branches and clumps of amyloid plaques between them

Stages of Alzheimer's Disease

Mild Cognitive Impairment (MCI)

Subtle memory or thinking problems noticeable but not interfering with daily life. About 15% of people over 65 with MCI develop dementia within 2 years5. A useful time to act; addressing risk factors is worthwhile, though no intervention has been shown to reliably prevent progression.

Mild to Moderate Alzheimer's

Recent memory loss, word-finding difficulty, disorientation, mood changes. Difficulty with complex tasks. Lasts 2 to 10 years. Patients gradually need more help.

Severe / Late-Stage

Loss of recognition of loved ones, language, mobility, swallowing. 24/7 care required. Death usually from pneumonia or other complications, typically 8 to 10 years after symptoms appear, though the course varies widely6.

Alzheimer's Disease by the Numbers

7.4 million
Americans aged 65 and older living with Alzheimer's in 2026, projected to reach nearly 13 million by 2050 7
~45%
of dementia cases worldwide are attributable to 14 modifiable risk factors, a population estimate rather than a promise for any one person4
~2/3
of Americans with Alzheimer's are women7
$409B
projected US health and long-term care costs for dementia in 2026, not counting the unpaid care families give7
60 to 70%
of dementia cases worldwide involve Alzheimer's disease; other forms include vascular, Lewy body and frontotemporal dementia3
14.9%
of people over 65 with mild cognitive impairment developed dementia within 2 years in the studies a neurology guideline reviewed5

Symptoms of Alzheimer's Disease

Memory loss is the classic and usually the earliest symptom, though in some people other cognitive domains decline first. Early recognition matters: memory problems can have other, treatable causes, and a diagnosis lets treatment and planning start8.

SymptomWhat happens
Cognitive Symptoms
Short-Term Memory LossForgetting recent conversations, repeating questions, misplacing items, missing appointments. The earliest and most prominent symptom. Long-term memories preserved early.
Word-Finding DifficultyPausing mid-sentence to search for words, substituting general terms ("thing" for specific items), trouble following conversations. Vocabulary shrinks.
Disorientation & Getting LostGetting lost in familiar places, confusion about time/date, difficulty following directions. Spatial navigation declines early.
Executive Function DeclineTrouble planning, managing finances, following recipes, problem-solving. Multi-step tasks become difficult. Bills go unpaid, finances mismanaged.
Behavioral & Functional
Mood & Personality ChangesDepression, anxiety, apathy, irritability. Withdrawal from hobbies and social activities. Personality changes; the person may become more or less outgoing than before.
Sleep Disturbances & SundowningDisrupted sleep-wake cycle. "Sundowning": confusion and agitation worsening in the late afternoon or evening. Reduced REM sleep impairs memory consolidation.
Agitation, Suspicion, HallucinationsIn later stages: paranoia (someone's stealing from me), hallucinations, agitation, wandering. Often distressing for caregivers.
Loss of Functional IndependenceProgressive inability to bathe, dress, toilet, eat, walk. Activities of Daily Living (ADLs) decline. Eventually 24/7 care needed.

Causes of Alzheimer's Disease

The causes are not fully understood; they probably combine age-related changes in the brain with genetic, health and lifestyle factors, and whether changing the lifestyle factors prevents dementia is not yet certain9.

CauseHow It Contributes to Alzheimer's DiseaseWhat Helps
AgeThe biggest known risk factor: about 1 in 13 people aged 65 to 84, and 1 in 3 aged 85 and older, live with Alzheimer's9Nothing changes age; memory changes still deserve an assessment, because other treatable conditions can cause them8
Genes and family historyThe APOE4 variant raises risk, though some carriers never develop the disease; a parent or sibling with Alzheimer's also raises risk, and rare variants in three genes cause it, usually before 65 9Genetic testing is optional and best done with counseling, as the diagnosis section says; the factors below apply whatever your genes
High blood pressure, diabetes, high LDL cholesterol and obesityVascular and metabolic conditions are studied as contributors9, and all four are on the Lancet Commission's list of modifiable risk factors4Treating blood pressure, blood sugar and cholesterol with your clinician, regular exercise, and the MIND or Mediterranean pattern in the diet section
Hearing and vision lossHearing loss is linked with higher risk9, and untreated vision loss joined the Commission's list in 2024 4Hearing tests and hearing aids (as the treatment section describes) and regular eye care
Inactivity, smoking, heavy drinking and social isolationEach is on the Commission's list; its level for harmful drinking is more than 12 US drinks a week4Regular exercise, stopping smoking, drinking less and staying socially connected, as the treatment section lists
Depression and head injuryDepression, and concussion or other traumatic brain injury, are linked with a higher risk9Getting depression treated, and helmets and fall prevention, as the treatment section lists

How Alzheimer's Disease Is Diagnosed

TestWhat it shows
Cognitive & Clinical Assessment
Cognitive Screening TestsMoCA (Montreal Cognitive Assessment), more sensitive than MMSE for early disease. MMSE (Mini-Mental State Exam). Mini-Cog (quick screening).
Comprehensive Neuropsychological Testing2 to 4 hour battery assessing memory, language, executive function, visuospatial skills. Most sensitive for early detection and differential diagnosis.
Brain MRIHippocampal atrophy, generalized cortical atrophy. Rules out other causes: strokes, tumors, normal pressure hydrocephalus, vascular dementia.
PET ImagingAmyloid PET, Tau PET, FDG-PET. Confirms Alzheimer's pathology in vivo. Expensive but increasingly available. New blood-based amyloid tests are emerging.
Modifiable Risk Workup
Metabolic PanelHbA1c and lipid panel. Diabetes and high LDL cholesterol are established, treatable risk factors; targets are set with your clinician.
B12, Folate, HomocysteineB12 deficiency mimics dementia and worsens it8. A homocysteine above 14 micromol per liter went with nearly double the risk of Alzheimer's disease in a cohort study10. Common MTHFR variants can raise homocysteine slightly; folic acid still works for people who carry them.
Vitamin D, Thyroid, Heavy MetalsLow vitamin D (below 20 ng/mL, or 50 nmol/L) went with a higher dementia risk in a cohort study, though supplements did not slow decline in a trial11, so a level is checked only where deficiency is suspected. Hypothyroidism mimics dementia. Test for heavy metals only if there is a specific known exposure.
APOE Genotype (Optional)APOE4 carriers (1 or 2 copies) have higher risk. Information allows earlier and more aggressive prevention. Ethical considerations, counseling recommended.

Conventional and Holistic Treatment for Alzheimer's Disease

๐ŸŒฟ HOLISTIC
๐Ÿ’Š CONVENTIONAL
๐ŸŒฟ

Holistic / Functional Approach

Address modifiable risk factors aggressively. The FINGER trial found a modest cognitive benefit from a multidomain lifestyle program.

Best Evidence
FINGER trial: two years of diet, exercise, cognitive training and vascular risk management, with a modest benefit to cognition
Prevention Power
~45% of cases attributable to 14 modifiable factors (Lancet Commission 2024)
Prevention Window
Risk factors act across the lifespan, including midlife12; pathology begins 15 to 20 years before symptoms1
For MCI
Addressing risk factors is worthwhile; no intervention has been shown to reliably prevent progression to dementia

Full Holistic Approach Includes

  • MIND diet or Mediterranean diet, associated with 35 to 53% lower Alzheimer's risk in one cohort study13, though a 3-⁠year randomized trial found no difference in cognition against a control diet14. Olive oil, leafy greens, berries, nuts, fatty fish, whole grains, beans.
  • Aerobic exercise 150+ min/week, linked with better brain health and hippocampal volume in studies.
  • Resistance training 2 to 3x/week: preserves muscle, glucose control, cognitive function
  • Sleep 7 to 9 hours/​night; the glymphatic system clears amyloid during deep sleep. Treat sleep apnea aggressively.
  • Social engagement: social isolation is one of the Lancet Commission's modifiable risk factors4.
  • Cognitive stimulation, learning new skills, languages, puzzles. Builds cognitive reserve.
  • Stress reduction, meditation, yoga, breathwork. Long-term stress raises cortisol, and cortisol that stays high has been linked with a smaller hippocampus in older adults32.
  • Optimize cardiometabolic health, BP below 130/80 (from age 80 the usual target is below 150/90, and with frailty or other conditions it is set by your clinician15), HbA1c below 5.7% and LDL below 100 mg/dL (2.6 mmol/L). These are prevention figures: if you take medicine for diabetes, your HbA1c goal is set with your clinician and is usually higher, and in someone living with dementia, pushing it down can do more harm than good16
  • Address hearing loss, among the largest and most treatable modifiable risk factors. Use hearing aids.
  • Quit smoking. Reduce alcohol (less is better and none is best): fewer than 7 drinks a week, or none
  • Address depression, one of the Lancet Commission's modifiable risk factors; get it treated4.
  • Avoid head injuries: helmets, fall prevention, caution with contact sports
  • Reduce air pollution exposure, HEPA filter at home, monitor outdoor AQI
โœ… What the evidence actually shows. The FINGER trial randomized 1,260 at-risk older adults to a multidomain program of diet, exercise, cognitive training and vascular risk management, and found a modest benefit to cognition. That is the strongest evidence in this area and it is worth acting on. A commercial protocol sold for Alzheimer's disease is often cited alongside it; it has been published as small uncontrolled case series, has not been tested against a control group, and should not be treated as equivalent. No intervention has been shown in a controlled trial to reverse established Alzheimer's disease. Addressing several modifiable factors together, and starting early, is still the best available approach.17

Evidence-Based Supplements for Alzheimer's Disease

No supplement has been shown to prevent or treat Alzheimer's disease; B vitamins matter mainly where there is a deficiency.

SupplementWhat it is forTypical rangeTimingNotes & cautions
Omega-⁠3 (EPA/DHA)DHA is part of nerve cell membranes, but randomized trials found no benefit to cognition, either in mild to moderate Alzheimer's disease or in healthy older adults22.Not recommended for Alzheimer's disease (reviews of the trials found no benefit)Not applicableEat fatty fish such as wild salmon or sardines instead. In heart trials, fish oil supplements raised the risk of atrial fibrillation, an irregular heartbeat, more so above 1 g a day23, so check any fish oil supplement with your clinician first.
Vitamin D3In a cohort study, vitamin D deficiency went with about 50% higher dementia risk, but in a randomized trial 2,000 IU a day did not slow cognitive decline over 2 to 3 years11. Receptors throughout brain. Anti-inflammatory.Not recommended for Alzheimer's disease (in a randomized trial, 2,000 IU a day did not slow cognitive decline)Not applicableIf your clinician finds a deficiency, it is treated for its own sake.
B-Complex (B12, B6, Folate)Lower homocysteine, which went with nearly double the Alzheimer's risk above 14 micromol per liter in a cohort study. In a trial in mild cognitive impairment, these B vitamins slowed brain shrinkage on scans by about 30%, and by about half when homocysteine was high; a scan change, not a proven benefit to memory10.B12 1,000 mcg + B6 20 mg + Folate 800 mcg/dayMorning with foodFolic acid works for people with MTHFR variants; methylfolate is an alternative, not a requirement. Test homocysteine.
CurcuminAnti-inflammatory and anti-amyloid in animal models, but in a 24-⁠week randomized trial in 36 people with Alzheimer's disease it showed no benefit on memory tests or brain markers24.Not recommended for Alzheimer's disease (the trial used 2 or 4 g a day)Not applicableStandard curcumin is poorly absorbed, and liver damage has been reported with the more absorbable forms: stop and see a clinician for tiredness, nausea, dark urine or yellowing skin25.
Lion's Mane MushroomIn one 16-⁠week trial in 30 older adults with mild cognitive impairment, cognitive scores improved and then fell within 4 weeks of stopping; it has not been tested in large trials26.1,000 to 3,000 mg/dayDivided dosesEffects diminish after stopping. Choose extracts standardized to beta-glucans/​hericenones.
PhosphatidylserineBrain membrane phospholipid. Evidence that it helps memory in early cognitive decline is very limited and preliminary.100 to 300 mg/dayWith mealsSunflower-derived preferred over soy.
Magnesium L-ThreonateMarketed for brain penetration; human evidence for cognitive benefit is limited.1,500 to 2,000 mg/day (2,000 mg provides ~144 mg elemental Mg)EveningPricey, and the evidence is limited. The upper intake level for supplemental magnesium is 350 mg/day; above that, diarrhea is common. With kidney disease, take it only on your clinician's advice.
Citicoline (CDP-Choline)Increases acetylcholine and phospholipid synthesis in laboratory work; not shown to prevent or treat Alzheimer's disease.250 to 1,000 mg/dayMorningWell-tolerated.

What to Expect Over Time

No treatment yet stops Alzheimer's disease; care aims to ease symptoms and keep independence for longer27.

Treatment and supportive care, together
First Weeks

Other causes of memory problems, such as depression, stress or medicines, are looked for first28. A cholinesterase inhibitor may be started; nausea, vomiting or poor appetite usually settle within 2 weeks28.

Months 1 to 3

In the United States, people with mild cognitive impairment or mild dementia due to Alzheimer's, with amyloid confirmed by a PET scan or spinal fluid test, may be offered an anti-amyloid antibody. In trials these slowed decline in some people over 18 months, and they need MRI checks for brain swelling or bleeding27.

Months 3 to 12

Cognitive stimulation, cognitive rehabilitation and life story work sit beside medicine28. Exercise, diet and blood pressure care continue; a combined program gave a modest cognitive benefit in a trial17.

Long Term

Symptoms progress slowly over several years, and in later stages people need help with eating, washing and dressing28. A different medicine class may be added for moderate to severe disease, and medicines for behavior come only after non-drug approaches27. Plan ahead while decisions are easier3.

When to Seek Care

Sudden confusion (delirium) needs emergency care now: call 911 or go to the ER, since infection, stroke or a medicine can cause it29. Call 911 for a drooping face, arm weakness or speech trouble, and after a fall with a possible head, back, neck or hip injury or when the person cannot get up29. If the person gets lost, call the police; a recent photo helps30. See a doctor promptly if symptoms worsen quickly28.

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Prevention Is Where the Leverage Is

Alzheimer's pathology begins 15 to 20 years before symptoms. The measures linked with lower risk (exercise, blood pressure and blood sugar care, hearing care, not smoking and staying socially connected) act across the lifespan, including midlife12. If you are in midlife, the time to begin is now.

References & Evidence Notes

Each numbered entry below is either a source you can follow or a note setting out what the evidence does and does not support. Both are numbered together so the markers in the text line up.

Last reviewed October 20, 2026. Supplement entries are cross-checked against the NIH National Center for Complementary and Integrative Health and the Linus Pauling Institute Micronutrient Information Center.31 Be careful in this area, because desperation and expensive protocols meet here. No intervention has been shown in a controlled trial to reverse established Alzheimer's disease. What the evidence does support is worth doing: managing cardiovascular risk, treating hearing loss, exercise, sleep, social and cognitive engagement, and not smoking are associated with lower dementia risk, and a multidomain program showed modest cognitive benefit in a large randomized trial. Be skeptical, in proportion to the price, of any protocol promising reversal, any supplement stack sold for memory and any clinic charging heavily for either. If cognitive change is new, get assessed: depression, thyroid disease, B12 deficiency, sleep apnea and medication effects all cause reversible cognitive impairment and are missed regularly.

  1. On what Alzheimer's is: a progressive neurodegenerative disease with amyloid plaques and tau tangles, beginning 15 to 20 years before symptoms. It is the most common cause of dementia but not the only one; vascular, Lewy body and frontotemporal dementias differ in presentation and management, and mixed pathology is common. ↩
  2. On supplements: no supplement has been shown to prevent or treat Alzheimer's disease. Ginkgo biloba failed in large prevention trials: in the GEM trial, 3,069 people aged 75 or older took 120 mg twice a day or placebo for a median of 6.1 years, and ginkgo did not reduce dementia or Alzheimer's disease, including in those who started with mild cognitive impairment, PubMed 19017911. Vitamin E has limited and inconsistent evidence in established disease and carries risk at high doses. B vitamins lower homocysteine with no reliable cognitive benefit except possibly where deficiency exists. Coconut oil, ketones and most memory formulations lack supporting trials. ↩
  3. On the forms of dementia and planning ahead: the World Health Organization states that Alzheimer's disease is the most common form of dementia and contributes to 60 to 70% of cases, with vascular, Lewy body and frontotemporal dementia among the other forms and mixed forms common; that no treatment ends it, but that a lot can be done to support people and those who care for them; and it advises planning ahead while decisions are easier, WHO, dementia. ↩
  4. On modifiable risk: the 2024 Lancet Commission lists 14 potentially modifiable risk factors for dementia (less education, hearing loss, high blood pressure, smoking, obesity, depression, physical inactivity, diabetes, drinking more than 12 US drinks a week, traumatic brain injury, air pollution, social isolation, untreated vision loss and high LDL cholesterol) and reports stronger evidence than before that tackling them reduces risk, PubMed 39096926. It estimates that about 45% of dementia cases worldwide are attributable to these factors, a population calculation that assumes the links are causal, PubMed 40823285. ↩
  5. On mild cognitive impairment: a neurology practice guideline found that 14.9% of people over 65 with mild cognitive impairment developed dementia over 2 years, that no high-quality evidence supports medicines for it, and that exercise training is likely to improve cognitive measures, PubMed 29282327. ↩
  6. On how long people live with the disease: MedlinePlus states that people with Alzheimer's disease usually survive 8 to 10 years after symptoms appear, but that the course of the disease can range from 1 to 25 years, MedlinePlus, Alzheimer disease. ↩
  7. On how many people are affected and at what cost: the Alzheimer's Association estimates that 7.4 million Americans aged 65 and older are living with Alzheimer's in 2026, projected to reach nearly 13 million by 2050; that almost two-thirds of Americans with Alzheimer's are women; and that health and long-term care costs for people with Alzheimer's and other dementias are projected to reach $409 billion in 2026, not including the value of unpaid care, Alzheimer's Association, Facts and Figures. ↩
  8. On reversible causes: looking for them is the first practical step. Depression, hypothyroidism, vitamin B12 deficiency, obstructive sleep apnea, alcohol, and anticholinergic and sedative medication all cause cognitive impairment that improves when addressed. A structured assessment looks for these, and finding one changes everything. ↩
  9. On causes: the National Institute on Aging states that the causes are not yet fully understood and probably combine age-related brain changes with genetic, health and lifestyle factors; that age is the biggest known risk factor, with about 1 in 13 people aged 65 to 84 and 1 in 3 aged 85 and older living with Alzheimer's; that the APOE4 variant raises risk but some carriers never develop the disease; that high blood pressure, diabetes, obesity, hearing loss, depression and head injury are linked with risk; and that researchers cannot yet say for certain whether changing lifestyle factors prevents dementia, NIA, what causes Alzheimer's disease. ↩
  10. On homocysteine: in a cohort of 1,092 older adults, a homocysteine level above 14 micromol per liter went with nearly double the risk of Alzheimer's disease, PubMed 11844848. In a 2-⁠year randomized trial in 168 people over 70 with mild cognitive impairment, folic acid 0.8 mg, vitamin B12 0.5 mg and vitamin B6 20 mg a day slowed brain shrinkage on MRI from 1.08% to 0.76% a year, and by 53% in those with homocysteine above 13; the trial measured scans, not whether dementia was delayed, PubMed 20838622. ↩
  11. On vitamin D and dementia: in a cohort of 1,658 older adults, vitamin D deficiency went with a higher risk of dementia (about 1.5 times with levels of 25 to 50 nmol/L, about 2.2 times below 25), rising most clearly below 50 nmol/L (20 ng/mL), PubMed 25098535. In a randomized trial in over 4,000 adults aged 60 and older, vitamin D3 at 2,000 IU a day did not slow cognitive decline over 2 to 3 years, PubMed 34853363. ↩
  12. On modifiable risk across the lifespan: the Lancet Commission's risk factors (listed in full in note 4) act at different stages of life, from less education in early life, through most of the factors in midlife, to social isolation, air pollution and untreated vision loss in later life, so lowering risk is worth starting in midlife or earlier. Hearing loss is among the largest and most treatable, and hearing aids are among the more concrete things available. ↩
  13. On the MIND diet cohort: in a Chicago study of 923 older adults followed for about 4.5 years, the highest third of MIND diet scores had a 53% lower rate of Alzheimer's disease and the middle third a 35% lower rate than the lowest third; this is an observational association, PubMed 25681666. ↩
  14. On diet: the MIND diet, combining Mediterranean and DASH elements, is associated with slower cognitive decline in observational cohorts. A randomized trial of the MIND diet published in N Engl J Med in 2023 found no significant difference in cognitive change compared with a mild calorie-restricted control, with both groups improving. The observational association is real; the trial did not confirm a specific effect. Eat this way for cardiovascular reasons, which are well supported, and treat cognitive benefit as unproven. ↩
  15. On blood pressure targets in older people: the NICE hypertension guideline sets a clinic target below 140/90 for most adults under 80 and below 150/90 for adults aged 80 and over, advises clinical judgment for people with frailty or multimorbidity, and advises checking for a drop in blood pressure on standing in people aged 80 and over, treating to a standing target where the drop is significant, NICE NG136. ↩
  16. On blood sugar targets: American College of Physicians guidance advises personal HbA1c goals for type 2 diabetes, an HbA1c between 7% and 8% for most people on treatment, easing treatment below 6.5%, and not targeting an HbA1c at all in people with dementia and a limited life expectancy, because the harms outweigh the benefits, PubMed 29507945. ↩
  17. On multidomain intervention, and on commercial protocols. The FINGER trial randomized 1,260 at-risk older adults to diet, exercise, cognitive training and vascular risk management, and found a modest benefit on cognitive performance; it is the strongest evidence in this area and the basis for taking the lifestyle approach seriously. A commercial protocol sold for Alzheimer's disease is frequently cited alongside it but has been published as small uncontrolled case series without a control group, and its results cannot be interpreted the same way. Presenting the two as equivalent evidence is not defensible, particularly where the protocol carries substantial cost. ↩
  18. On new drug treatments: anti-amyloid monoclonal antibodies slow decline modestly in early disease, with meaningful risks including brain swelling and microhemorrhage, substantial cost and demanding monitoring. Whether the benefit is clinically noticeable is genuinely debated. This belongs with a specialist rather than in a supplement discussion. ↩
  19. On the size of the anti-amyloid effect: in the main 18-⁠month trial of one anti-amyloid antibody in 1,795 people with early Alzheimer's disease, decline on a dementia rating scale was 0.45 points smaller than on placebo on an 18-⁠point scale, which the investigators described as moderately less decline; infusion reactions occurred in 26.4% and brain swelling or fluid on MRI in 12.6%, PubMed 36449413. ↩
  20. Morris MC, Wang Y, Barnes LL, Bennett DA, Dawson-Hughes B, Booth SL. Nutrients and bioactives in green leafy vegetables and cognitive decline: prospective study. Neurology. 2018;90(3):e214-⁠e222. PubMed 29263222. In 960 older adults followed for a mean 4.7 years, those in the highest fifth of green leafy vegetable intake (median 1.3 servings a day) had a slower rate of cognitive decline, the equivalent of being 11 years younger in age; this is an observational association. ↩
  21. Devore EE, Kang JH, Breteler MM, Grodstein F. Dietary intakes of berries and flavonoids in relation to cognitive decline. Ann Neurol. 2012;72(1):135-⁠143. PubMed 22535616. In 16,010 women aged 70 and older in the Nurses' Health Study, greater intakes of blueberries and strawberries were associated with slower rates of cognitive decline, an effect the authors estimated at up to 2.5 years of cognitive aging; this is an observational association. ↩
  22. On omega-⁠3 and cognition: a Cochrane review of three randomized trials in 632 people with mild to moderate Alzheimer's disease found no benefit of omega-⁠3 supplements on cognition, daily function or dementia severity (high-quality evidence), PubMed 27063583, and an earlier Cochrane review of trials in cognitively healthy older people found no cognitive benefit either, PubMed 22696350. ↩
  23. Gencer B, Djousse L, Al-Ramady OT, Cook NR, Manson JE, Albert CM. Effect of long-term marine omega-⁠3 fatty acids supplementation on the risk of atrial fibrillation in randomized controlled trials of cardiovascular outcomes: a systematic review and meta-analysis. Circulation. 2021;144(25):1981-⁠1990. PubMed 34612056. Seven trials with 81,210 people followed for about 5 years: omega-⁠3 supplements were linked to a higher risk of atrial fibrillation (hazard ratio 1.25), more so in trials of more than 1 g a day (1.49), and the risk rose with each additional gram. ↩
  24. On curcumin: in a 24-⁠week randomized trial in 36 people with mild to moderate Alzheimer's disease, curcumin at 2 or 4 g a day showed no clinical or biomarker benefit over placebo, and blood levels stayed low, PubMed 23107780. ↩
  25. On curcumin safety: NIH's complementary health center reports that liver damage has been reported in some people taking the more absorbable curcumin formulations, and advises stopping and seeing a clinician for tiredness, nausea, poor appetite, dark urine or yellowing of the skin, NCCIH, turmeric. ↩
  26. On lion's mane: in a 16-⁠week placebo-controlled trial in 30 Japanese adults aged 50 to 80 with mild cognitive impairment, cognitive scores rose on the mushroom powder and fell again within 4 weeks of stopping; it has not been tested in large trials, PubMed 18844328. ↩
  27. On treatment: the National Institute on Aging states that no known treatment ends Alzheimer's disease; that cholinesterase inhibitors are prescribed for mild to moderate symptoms and an NMDA antagonist for moderate to severe disease; that two anti-amyloid antibodies are approved in the United States for mild cognitive impairment or mild dementia due to Alzheimer's, after a PET scan or spinal fluid test confirms amyloid, and slowed decline in some trial participants over 18 months; that they can cause fluid buildup or bleeding in the brain, occasionally serious, so MRI monitoring is needed; and that medicines for behavior should be used only after non-drug approaches, NIA, how Alzheimer's disease is treated. ↩
  28. On the course of the disease and care: NHS guidance states that symptoms progress slowly over several years at a different rate for each person; that memory problems can also be caused by depression, stress, medicines or other health problems; that anyone whose symptoms are rapidly getting worse should be seen by a doctor; that side effects of the symptom medicines, such as nausea, vomiting and loss of appetite, usually improve after 2 weeks; and that cognitive stimulation therapy, cognitive rehabilitation and reminiscence and life story work are part of care, NHS, Alzheimer's symptoms, NHS, Alzheimer's treatment. ↩
  29. On emergencies: NHS guidance advises going to an emergency department or calling emergency services if someone suddenly becomes confused, since causes include infection, stroke and some prescription medicines, and calling emergency services after a fall with a possible head, back, neck or hip injury or when the person cannot get up; the CDC advises calling 911 at once for a drooping face, a drifting arm or slurred or strange speech, NHS, sudden confusion, NHS, falls, CDC, stroke signs. ↩
  30. On getting lost: the National Institute on Aging advises that the person carries ID or a medical bracelet, that neighbors and local police know the person tends to wander, and that a recent photograph is kept to help police if the person becomes lost, NIA, wandering and getting lost. ↩
  31. National Center for Complementary and Integrative Health (NIH), nccih.nih.gov, and the Linus Pauling Institute Micronutrient Information Center, lpi.oregonstate.edu/mic. ↩
  32. On stress and the hippocampus: a 1998 study in Nature Neuroscience by Lupien and colleagues found that older adults whose cortisol, a stress hormone, stayed high over several years had a smaller hippocampus and poorer memory than those with normal cortisol, PubMed 10195112. ↩