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.

Tarenflurbil did not slow cognitive decline or the loss of activities of daily living in patients with mild AD. 3 key findings →

Design: clinical trial Participants: 1,684 Evidence: high

The Alzheimer's Disease Neuroimaging Initiative (ADNI) aims to validate biomarkers for Alzheimer's disease (AD) clinical trials. 1 key finding →

Design: longitudinal study Participants: 20,000 Evidence: moderate

Naproxen and celecoxib do not prevent AD in early results from a randomized controlled trial

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Neurology 2007-04-25

These results do not support the hypothesis that celecoxib or naproxen prevent Alzheimer dementia, at least within the early years after initiation of treatment. 2 key findings →

Evidence: high

The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Participants: 400 Evidence: moderate

Among the 158 participants who accurately recalled their Alzheimer disease risk assessment 6 weeks after risk disclosure, 75 (47.5%) believed their Alzheimer disease risk was more than 5% points different from the Alzheimer disease risk estimate they were given. 2 key findings →

Design: randomized controlled trial Participants: 158 Evidence: high

Diabetes mellitus and risk of developing Alzheimer disease: results from the Framingham Study

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Archives of neurology 2006-11-01

Diabetes mellitus did not increase the risk of incident AD in the Framingham cohort overall; however, DM may be a risk factor for AD in the absence of other known major AD risk factors. 3 key findings →

Design: cohort study Participants: 2,210 Evidence: moderate

These studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design. 2 key findings →

Design: longitudinal study Evidence: moderate

This article reviews all papers published since the inception of the initiative and summarizes the results as of February 2011. 1 key finding →

Design: longitudinal study Participants: 400 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

A condensed protocol for communicating genetic risk for Alzheimer disease achieved similar educational results as an extended protocol in this study. 3 key findings →

Participants: 280 Evidence: high

Head injury and the risk of AD in the MIRAGE study

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2000-03-01

Comparison of probands with their unaffected spouses yielded odds ratios for AD of 9.9 (95% CI, 6.5 to 15.1) for head injury with loss of consciousness and 3.1 (2.3 to 4.0) for head injury without loss of consciousness. 3 key findings →

Participants: 2,233 Evidence: low

(1) Data-driven AD progression models supported multifactorial interactions rather than a linear cascade of events. 4 key findings →

Design: longitudinal study Evidence: high

Depression as a risk factor for Alzheimer disease: the MIRAGE Study

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Archives of neurology 2003-05-01

Depression symptoms before the onset of AD are associated with the development of AD, even in families where first depression symptoms occurred more than 25 years before the onset of AD. 4 key findings →

Design: case-control study Participants: 1,953 Evidence: moderate

Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →

Design: case-control study Participants: 338 Evidence: moderate

Progression of Alzheimer dementia (AD) is highly variable. 4 key findings →

Design: cohort study Evidence: moderate

Risk of dementia among white and African American relatives of patients with Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA 2002-01-01

However, in this study, the additional risk of dementia conferred by being a first-degree relative, by being female, or by the probability of having an APOE epsilon4 allele appeared similar in African American and white families. 1 key finding →

Participants: 17 Evidence: low

Conversion to dementia from mild cognitive disorder: the Cache County Study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2006-07-01

Individuals with all types of mild cognitive impairment have an elevated risk of dementia over 3 years, more so in those with an APOE epsilon4 allele. 3 key findings →

Participants: 120 Evidence: low

ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →

Evidence: low

The Framingham Brain Donation Program: neuropathology along the cognitive continuum

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Current Alzheimer research 2012-07-01

The Framingham Heart Study has enrolled 3 generations of participants, the original cohort (gen 1) enrolled in 1948, the offspring cohort (gen 2) enrolled in 1971 and the third generation enrolled in 2002. 4 key findings →

Participants: 59 Evidence: moderate

APOE, vascular pathology, and the AD brain

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurology 2005-07-01

APOE-epsilon4 is associated with small vessel arteriolosclerosis, microinfarcts of the deep nuclei, neuritic senile plaque density, and amyloid angiopathy in patients with autopsy-proven Alzheimer disease (AD). 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 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