Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

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In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Ginkgo biloba for preventing cognitive decline in older adults: a randomized trial

✓ Peer-reviewed alzhub usefulness score 79 out of 100. JAMA 2009-12-01

Compared with placebo, the use of G. biloba, 120 mg twice daily, did not result in less cognitive decline in older adults with normal cognition or with mild cognitive impairment. 3 key findings →

Participants: 1,545 Evidence: high

In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified. 4 key findings →

Design: meta-analysis Participants: 2,784 Evidence: high

Using cross-population GWAS meta-analyses, we identify novel LOAD susceptibility loci in/near LRRC4C and LHX5-AS1, both with known roles in neuronal development, as well as several novel population-unique loci. 1 key finding →

Design: meta-analysis Participants: 409,589 Evidence: high

Baseline levels of LD Aβ were greater for adults with mild cognitive impairment compared with adults with normal cognition (LD Aβ42, P = .05; LD Aβ40, P = .01). 3 key findings →

Evidence: high

The development of MCI is associated with measurements of cognition and depression, racial and constitutional factors, and cerebrovascular disease. 5 key findings →

Design: longitudinal study Participants: 927 Evidence: moderate

Circulating homocysteine levels (tHcy), a product of the folate one carbon metabolism pathway (FOCM) through the demethylation of methionine, are heritable and are associated with an increased risk of common diseases such as stroke, cardiovascular disease (CVD), cancer and dementia. 4 key findings →

Design: meta-analysis Participants: 2,710 Evidence: high

Incidence and prevalence of dementia in the Cardiovascular Health Study

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Journal of the American Geriatrics Society 2004-02-01

Classification resulted in 227 persons with prevalent dementia at entry into the study and 480 incident cases during follow-up. 4 key findings →

Design: cohort study Participants: 227 Evidence: moderate

Cognitive resilience to apolipoprotein E ε4: contributing factors in black and white older adults

✓ Peer-reviewed alzhub usefulness score 61 out of 100. JAMA neurology 2015-03-01

Although APOE ε4 carriers are at high risk for cognitive decline, our findings suggest possible intervention targets, including the enhancement of cognitive reserve and improvement of other psychosocial and health factors, to promote cognitive resilience among black and white APOE ε4 carriers. 5 key findings →

Design: prospective cohort Participants: 2,487 Evidence: moderate

Among the 183 study participants, mean (SD) age was 85.5 (3) years, 76 were women (41.5%), and 177 were white (96.7%). 4 key findings →

Design: cross-sectional Participants: 183 Evidence: low

Admixture mapping identifies novel Alzheimer's disease risk regions in African Americans

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Alzheimer's & Dementia 2022-12-20

Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus. 5 key findings →

Design: case-control Participants: 10,271 Evidence: moderate

Down syndrome (DS), or trisomy 21, is a common disorder associated with several complex clinical phenotypes. 1 key finding →

Participants: 30 Evidence: low

Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →

Design: cohort Evidence: high

Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD). 1 key finding →

Evidence: moderate

Significant association between SCN8A and Alzheimer disease in Puerto Ricans

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Alzheimer s & Dementia 2025-12-01

) within the first intron of SCN8A on chromosome 12 (Figure 1), overlapping a significant region in the previous admixture mapping analysis. eHiCA revealed more and stronger interactions between rs4761988 and SLC4A8, SCN8A and FIGNL2 in EU compared to AF genome (Figure 2), consistent with the admixture mapping result. 4 key findings →

Design: meta-analysis Participants: 867 Evidence: high

Benefits of fatty fish on dementia risk are stronger for those without APOE epsilon4

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Neurology 2005-11-01

In the Cardiovascular Health Cognition Study, consumption of fatty fish was associated with a reduced risk of dementia and Alzheimer disease for those without the APOE epsilon4 allele. 2 key findings →

Evidence: low

Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts. 1 key finding →

Design: cross-sectional Participants: 751 Evidence: early

Plasma phosphorylated threonine 181 of tau (pTau181) and amyloid beta (Aβ) are biomarkers for differential diagnosis and preclinical detection of Alzheimer disease (AD). 2 key findings →

Participants: 2,086 Evidence: low

Polygenic Risk Scores for Incident Dementia in the Multi‐Ethnic Study of Atherosclerosis

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Genetic Epidemiology 2026-06-23

We found comparable associations between dementia and PRS when comparing a C+T method with only 15 SNPs and PRS derived from Bayesian models that include > 800,000 SNPs (HR 5e‐08 = 1.18, 95% CI: 1.08–1.28; HR CSx = 1.17, 95% CI: 1.07−1.27). 3 key findings →

Evidence: low

Heterogeneity in the Genetic Architecture of Alzheimer disease (AD) across Ancestry Groups

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Alzheimer s & Dementia 2025-12-01

Overall SNP‐based heritability estimates using this restricted set of variants varied: AA ( h 2 = 0.13, SE=0.05), NHW ( h 2 = 0.14, SE=0.01), AsA ( h 2 = 0.29, SE=0.09) and HL ( h 2 = 0.48, SE=0.17). 2 key findings →

Participants: 6,343 Evidence: low

Alzheimer Disease (AD) is a highly polygenic dementia that presents with relatively earlier onset (≤65yo; EOAD) in about 5% of cases. 2 key findings →

Participants: 15 Evidence: low

Discordance Between Genetic Ancestry and Self-Reported Race Impacts Inference of Neuropsychiatric Burden in Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-26

IntroductionNeuropsychiatric symptoms (NPS)--including aggression, psychosis, anxiety, apathy, and depression--affect up to 85% of individuals with Alzheimers disease (AD) and are among its most disabling and costly manifestations, accelerating cognitive and functional decline, institutionalization, mortality, and healthcare costs. 1 key finding →

Evidence: low

We investigated associations of neighborhood disadvantage with Alzheimer's Disease (AD)-related outcomes by biological and social factors in at-risk older adults. 1,880 U.S. POINTER participants with Area Deprivation Index (ADI) and cognition (PACC) were included. 868 had amyloid, tau PET, white matter hyperintensities (WMH), and/or gray matter volumes. 5 key findings →

Evidence: low

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Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 28,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed