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.

  • 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.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

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.

Cohort Profile Update: The Lothian Birth Cohorts of 1921 and 1936

✓ Peer-reviewed alzhub usefulness score 64 out of 100. International Journal of Epidemiology 2018-01-29

By wave, compared with those who remained in the LBC1921 study at Waves 1 to 5, participants who dropped out had: significantly lower older-age IQ scores at Wave 1 Wave 2 = and Wave 3 = lower scores at Waves and at Waves 1 = and 2 = By wave, compared with those who remained in the LBC1936 study at Waves 1 to participants who dropped out had: significantly lower older-age IQ scores at Wave 1 Wave 2 = and Wave 3 = lower scores at Wave 1 = Wave 2 and Wave 3 = lower at Wave 1 = Wave 2 = and Wave 3 and lower physical as at Wave 1 Wave 2 = and Wave 3 = and at Wave 1 = at each wave in the Lothian Birth Cohort 1921 are mean and standard for and for each wave sample = Wave 1 = Waves 1 and 2 = Waves 2 and 3 = Waves IQ from Moray House Test for age in at time of testing and to IQ is the was from to from the in 1 and at Wave 1. as of from the Wave 2 two participants who not Wave 1. 1 key finding →

Design: longitudinal study Participants: 87 Evidence: moderate

The apolipoprotein E (APOE) gene is the best established genetic risk factor for Alzheimer's disease in later life, with the ε4 allele conferring higher risk. 5 key findings →

Design: cohort Participants: 9,496 Evidence: moderate

Female individuals had higher plaque burden than male individuals (unadjusted odds ratio [OR], 1.97; 95% CI, 1.67-2.29; P Conclusions and relevance The findings indicate that female sex, APOEε4, and both race and African ancestry were jointly associated with amyloid in this study population. 3 key findings →

Design: cross-sectional Participants: 2,268 Evidence: moderate

Age, Sex, and APOE ε4 Effects on Memory, Brain Structure, and β-Amyloid Across the Adult Life Span

✓ Peer-reviewed alzhub usefulness score 63 out of 100. JAMA neurology 2015-05-01

Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. 5 key findings →

Design: cross-sectional Participants: 1,246 Evidence: low

We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers. 1 key finding →

Design: cohort study Evidence: moderate

Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →

Design: cross-sectional Participants: 567 Evidence: moderate

Association of Chronic Low-grade Inflammation With Risk of Alzheimer Disease in ApoE4 Carriers

✓ Peer-reviewed alzhub usefulness score 63 out of 100. JAMA network open 2018-10-05

Median (interquartile range) CRP levels increased with mean (SD) age (43.3 [9.6] years, 0.95 mg/L [0.40-2.35 mg/L] vs 59.1 [9.6] years, 2.04 mg/L [0.93-4.75 mg/L] vs 61.6 [9.5] years, 2.21 mg/L [1.05-5.12 mg/L]; P Conclusions and relevance In this study, peripheral chronic low-grade inflammation in participants with ApoE4 was associated with shortened latency for onset of AD. 2 key findings →

Design: cohort study Evidence: moderate

Risk information for Alzheimer disease (AD) may be communicated through susceptibility gene disclosure, even though this is not currently in clinical use. 2 key findings →

Evidence: high

Statin therapy and risk of dementia in the elderly: a community-based prospective cohort study

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neurology 2004-11-01

Employing time-dependent proportional hazards modeling, the authors found no significant association between statin use and incident dementia or probable AD. 2 key findings →

Design: cohort study Participants: 312 Evidence: moderate

Polygenic Overlap Between C-Reactive Protein, Plasma Lipids, and Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Circulation 2015-04-10

By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD. 3 key findings →

Evidence: low

Relationship of regional brain β-amyloid to gait speed

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neurology 2015-12-07

More research is needed to elucidate the neural mechanisms underlying these regional associations, which may involve motor and sensorimotor circuits hitherto largely neglected in the pathophysiology of AD. 1 key finding →

Design: cross-sectional Evidence: low

Genetic variants within the VCAN gene may play a role in the mechanisms underlying microstructural integrity of the white matter in the brain measured as FA and MD. 4 key findings →

Design: cohort study Participants: 8,448 Evidence: moderate

Advances in genetic research have provided a basis for susceptibility testing for Alzheimer disease (AD). 2 key findings →

Design: randomized controlled trial Participants: 160 Evidence: high

44 participants were included: 20 PSEN1 E280A mutation carriers and 24 non-carriers. 2 key findings →

Participants: 44 Evidence: moderate

The exact etiology of dementia is still unclear, but both genetic and lifestyle factors are thought to be key drivers of this complex disease. 1 key finding →

Participants: 6,352 Evidence: low

Amyloid is linked to cognitive decline in patients with Parkinson disease without dementia

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neurology 2012-12-12

At baseline measurements, amyloid burden does not distinguish between cognitively impaired and unimpaired subjects with PD without dementia, but our data suggest that amyloid contributes to cognitive, but not motor, decline over time. 3 key findings →

Design: cohort study Participants: 46 Evidence: moderate

Strikingly gene-expression, network-based analysis and cell type deconvolution approaches revealed a consistent immune signature in the brain and blood of female AD patients that was absent in males. 5 key findings →

Design: meta-analysis Evidence: high

A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neuron 2011-09-21

The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases. 2 key findings →

Evidence: low

From across this tag

10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ Change the filters

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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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