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  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
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These counts and lists are worked out from the library itself each time the page loads. A score rates how much weight a study can bear — its design, journal, evidence and recency — not whether its result is good news. The study type is the one each record states; a record with no stated design is not counted here.

The 20 highest-scoring

  1. APOE Genotype and Alzheimer Disease Risk Across Age, Sex, and Population Ancestry JAMA Neurology · 2023-12-01 · · Peer-reviewed

    In 68,756 East Asian, Hispanic, Black and White individuals, links between APOE genotype and Alzheimer disease differed by ancestry: the ε2 genotypes (ε2/ε2, ε2/ε3) showed no association with AD in East Asian people (OR 0.97), and Hispanic people showed weaker APOE associations that overall ancestry could not explain. A previously reported higher risk for women with the ε3/ε4 genotype was seen again in White individuals, but at ages 60 to 70 (OR 1.48), and also in a combined analysis of Black and Hispanic individuals (OR 1.72). These are statistical associations; they do not give anyone a personal risk figure and do not point to a treatment.

  2. Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease Nature genetics · 2017-07-17 · · Peer-reviewed

    In a three-stage genetic study of 85,133 people, the authors found three new protein-changing variants linked to Alzheimer's disease, including "a protective variant in PLCG2" (odds ratio 0.68, rarer in people with Alzheimer's than in controls) and "a risk variant in ABI3". The authors say the findings "implicate microglial-mediated innate immunity", meaning the brain's immune cells. These are rare-variant associations, not causes, and the study tests no treatment or prevention.

  3. Endophenotype-based in silico network medicine discovery combined with insurance record data mining identifies sildenafil as a candidate drug for Alzheimer's disease Nature aging · 2021-12-06 · · Peer-reviewed
  4. A cerebrospinal fluid synaptic protein biomarker for prediction of cognitive resilience versus decline in Alzheimer's disease Nature medicine · 2025-03-31 · · Peer-reviewed

    Using cerebrospinal fluid proteomics in 3,397 individuals, the ratio YWHAG:NPTX2 explained variance in cognitive impairment beyond amyloid-beta and tau measures and predicted conversion from cognitively normal to mild cognitive impairment and from mild cognitive impairment to dementia. It is described as a prognostic biomarker, not a treatment, cure, or prevention.

  5. UK Biobank: An Open Access Resource for Identifying the Causes of a Wide Range of Complex Diseases of Middle and Old Age PLoS Medicine · 2015-03-31 · · Peer-reviewed

    UK Biobank is a large prospective study with over 500,000 participants that collects extensive health data and is openly available to researchers. It provides a resource for studying the causes of complex diseases of middle and old age, including Alzheimer's.

  6. Exposure to Air Pollutants and Lewy Body and Parkinson Disease-Related Dementias JAMA network open · 2026-05-01 · · Peer-reviewed
  7. Association of Plasma Neurofilament Light With Neurodegeneration in Patients With Alzheimer Disease JAMA neurology · 2017-05-01 · · Peer-reviewed

    In people with Alzheimer's dementia and mild cognitive impairment, plasma neurofilament light was higher and correlated with CSF neurofilament light and other markers. This supports it as a blood marker of nerve damage, not a treatment or cure.

  8. Sex modifies the APOE-related risk of developing Alzheimer disease Annals of neurology · 2014-04-14 · · Peer-reviewed

    In 5,496 healthy older adults, carriers of the APOE4 gene variant were more likely to develop mild cognitive impairment or Alzheimer's, and the increase was larger in women than in men (hazard ratio 1.81 vs 1.27). Among 2,588 people who already had MCI, APOE4 raised the risk of progressing to Alzheimer's in both sexes (2.16 vs 1.64), but the sex difference was not statistically significant unless the analysis was limited to people with the APOE3/3 or 3/4 genotypes. In 980 ADNI participants, the APOE4 effect on spinal-fluid tau was more Alzheimer's-like in women with MCI, which the authors say "may be associated" with women's higher risk; this is an association, and the study tested no treatment.

  9. Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis JAMA neurology · 2017-10-01 · · Peer-reviewed

    This analysis of many studies found that men and women with the APOE ε3/ε4 genotype have nearly the same odds of developing Alzheimer's disease from age 55 to 85, though women had higher risk at younger ages. It also found no significant difference between men and women in converting from mild cognitive impairment to Alzheimer's disease.

  10. Anticholinergic Drug Exposure and the Risk of Dementia: A Nested Case-Control Study JAMA internal medicine · 2019-08-01 · · Peer-reviewed

    This nested case-control study found that higher cumulative exposure to anticholinergic drugs was associated with increased dementia risk. It identifies a possible modifiable risk factor, but does not show that avoiding these drugs prevents Alzheimer's disease.

  11. Variant of TREM2 associated with the risk of Alzheimer's disease The New England journal of medicine · 2012-11-14 · · Peer-reviewed

    This genetic study sequenced the genomes of 2,261 Icelanders to look for rare variants likely to affect protein function. It then tested those variants in people with and without Alzheimer's disease, and checked them in case-control groups from the United States, Norway, the Netherlands and Germany. The authors report a TREM2 variant associated with Alzheimer's disease risk, but the summary held here stops before the results, so see the original paper for which variant and how large the effect is. It identifies a genetic risk association and does not test any treatment, cure, or prevention.

  12. Association of African Ancestry-Specific APOE Missense Variant R145C With Risk of Alzheimer Disease JAMA · 2023-02-21 · · Peer-reviewed

    In 2,888 people with Alzheimer's and 4,957 controls of African ancestry, those with the ε3/ε4 APOE genotype who also carried a variant called R145C had about 3 times the odds of Alzheimer's (odds ratio 3.01) and a reported onset about 6 years earlier. The link was not seen in other APOE genotypes, and a second variant, R150H, showed no association. The authors call this exploratory and say external validation is needed before it could inform genetic risk assessment for people of African ancestry.

  13. The Association between Social Engagement, Loneliness, and Risk of Dementia: A Systematic Review and Meta-Analysis Journal of Alzheimer's disease : JAD · 2018-01-01 · · Peer-reviewed

    This meta-analysis found that poor social engagement, such as a poor social network or poor social support, was associated with increased dementia risk, while loneliness was not significantly associated with increased risk. The authors suggest interventions targeting social isolation for dementia prevention, but this review does not test such interventions.

  14. Rare genetic variation in fibronectin 1 (FN1) protects against APOEε4 in Alzheimer's disease Acta Neuropathologica · 2024-04-10 · · Peer-reviewed

    This study found that rare variants in the FN1 gene may reduce Alzheimer risk related to APOE ε4, and zebrafish experiments suggested fibronectin loss-of-function reduced gliosis and improved clearance of toxic proteins. The work points to the extracellular matrix as a possible target, but it is early laboratory and genetic research, not a treatment.

  15. Alzheimer Disease Blood Biomarkers in Patients With Out-of-Hospital Cardiac Arrest JAMA neurology · 2023-04-01 · · Peer-reviewed

    In people who had out-of-hospital cardiac arrest, serum p-tau rose early in those with poor neurological outcome and then fell, while amyloid-beta levels rose over time in most patients. These Alzheimer-related blood markers changed after cardiac arrest but were only weakly linked to neurological outcome, and the study did not test any Alzheimer treatment.

  16. Genome-wide haplotype association study identifies the FRMD4A gene as a risk locus for Alzheimer's disease Molecular psychiatry · 2012-03-20 · · Peer-reviewed
  17. Common variants in Alzheimer's disease and risk stratification by polygenic risk scores Nature communications · 2021-06-07 · · Peer-reviewed
  18. Antipsychotics, other psychotropics, and the risk of death in patients with dementia: number needed to harm JAMA psychiatry · 2015-05-01 · · Peer-reviewed

    In 90,786 veterans aged 65 or older with dementia, this study set out to measure how much a new prescription for an antipsychotic changes the absolute risk of death over 180 days. For haloperidol, death risk was 3.8 percentage points higher than in matched people not taking the drug (95% CI 1.0–6.6), and the authors conclude the absolute effect of antipsychotics "may be higher than previously reported and increases with dose." This is an observational association, not proof of cause, and it is a reason to discuss risks and alternatives with the prescriber, not to stop a medication without advice.

  19. Anticholinergic drugs and risk of dementia: case-control study BMJ (Clinical research ed.) · 2018-04-25 · · Peer-reviewed

    Longer and heavier use of certain anticholinergic drugs, especially antidepressants, urological, and antiparkinson drugs, was linked to a modestly higher risk of developing dementia. This was an observational case-control study, so it cannot prove that these drugs cause dementia.

  20. Midlife overweight and obesity increase late-life dementia risk: a population-based twin study Neurology · 2011-05-01 · · Peer-reviewed

    Among 8,534 Swedish twins, people who were overweight or obese around age 43 had higher odds of dementia after 65 (odds ratios 1.71 and 3.88 versus BMI 20–25). When twins were compared with their own co-twin in 137 pairs, the link was weaker, which the authors say suggests genes and early-life environment explain part of it. This is an association from observational data; the study did not test whether changing weight changes dementia risk.

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