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.

Further studies are warranted to develop and refine the specific MIND diet for different populations. 4 key findings →

Design: meta-analysis Participants: 224,049 Evidence: moderate

Our findings suggest that higher adherence to the MIND diet was associated with better cognitive function and potentially slower cognitive decline in later life. 4 key findings →

Design: meta-analysis Participants: 4,066 Evidence: high

In a study of 2.2 million adults in Ontario, Canada, people who lived very close to a major road (within 50 meters) had a small but statistically significant higher risk of developing dementia than those living farther away (over 300 meters), even after accounting for other health and demographic factors. 4 key findings →

Design: cohort Participants: 2,200,000 Evidence: high

Between 2001, and 2012, we identified 243 611 incident cases of dementia, 31 577 cases of Parkinson's disease, and 9247 cases of multiple sclerosis. 3 key findings →

Design: cohort study Evidence: moderate

Smoking Cessation, Weight Change, and Risk of Dementia: A Prospective Cohort Study

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurology 2026-05-20

Smoking cessation was associated with a sustained lower dementia risk and slower cognitive decline, comparable to never smokers and those without short-term risk increase. 5 key findings →

Design: cohort Participants: 32,802 Evidence: moderate

Oral benfotiamine is safe and potentially efficacious in improving cognitive outcomes among persons with MCI and mild AD. 5 key findings →

Design: randomized controlled trial Evidence: low

Our findings suggest that poor olfaction is associated with multiple AD-related and other neurodegenerative processes. 5 key findings →

Design: cross-sectional Participants: 1,545 Evidence: moderate

These results indicate that trans-resveratrol has potential neuroprotective roles in the treatment of moderate to mild AD and that its mechanism may involve a reduction in the accumulation and toxicity of Aβ in the brain of patients, thereby reducing neuroinflammation. 4 key findings →

Design: case-control study Participants: 15 Evidence: moderate

Triggering receptor expressed on myeloid cells-2 (TREM2) is a key pro-tumorigenic marker of tumor-infiltrating macrophages, showing potent immunosuppressive activity in tumor microenvironment. 3 key findings →

Evidence: low

Mild cognitive impairment in Parkinson's disease research has progressed from basic mechanism exploration to a multidisciplinary, integrated clinical-basic stage, following an evolutionary path of "pathological mechanism - clinical phenotype - biomarker - intervention strategy." 2 key findings →

Design: systematic review Evidence: low

Presenilin 1 is required for Notch1 and DII1 expression in the paraxial mesoderm

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1997-05-01

Approximately 10% of cases of Alzheimer's disease are familial and associated with autosomal dominant inheritance of mutations in genes encoding the amyloid precursor protein, presenilin 1 (PS1) and presenilin 2 (PS2). 2 key findings →

Evidence: low

Blood-biomarker-based tests are highly important for the early clinical diagnosis of Alzheimer's disease (AD) and the treatment and care of AD patients, but the complex serum environment and extremely low abundance of AD blood protein biomarkers present challenges. 1 key finding →

Evidence: low

Focused Ultrasound-mediated Liquid Biopsy in a Tauopathy Mouse Model

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Radiology 2023-01-31

In the 2-month-old mice, sonobiopsy significantly increased the normalized levels of plasma p-tau species compared with the conventional blood-based liquid biopsy (p-tau-181-to-mouse tau [m-tau] ratio: 1.7-fold increase, P = .006; p-tau-231-to-m-tau ratio: 1.4-fold increase, P = .048). 1 key finding →

Evidence: low

However, recent data suggest that the risk of adverse effects may offset the benefits of atypical agents in patients with dementia. 5 key findings →

Evidence: low

Recent studies have indicated an association between Alzheimer's disease (AD) and central nervous system (CNS) insulin resistance. 4 key findings →

Evidence: low

Disease stage-sensitive MFSD2A-caveolae axis insigates hippocampal blood–brain barrier disruption in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-08

Blood-brain barrier (BBB) malfunction contributes to pathophysiology of Alzheimer’s disease (AD), yet the mechanisms that confer hippocampal endotheliocytes vulnerability remain unclear. 2 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