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.

After adjusting for demographics, apolipoprotein E (APOE) ε4 status, cognition, and comorbidities, the highest tertile of REM latency was associated with higher Aβ burden (β = 0.08, 95% confidence interval [CI]: 0.03 to 0.13, p = 0.002), elevated p-tau181 (β = 0.19, 95% CI: 0.02 to 0.13, p = 0.002), and reduced BDNF levels (β = -0.47, 95% CI: -0.68 to -0.13, p = 0.013), compared to the lowest tertile. 5 key findings →

Participants: 128 Evidence: low

The Relationship Between Sleep, Cognition, and Dementia Risk in People With Focal Epilepsy

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurology 2026-04-22

= 0.991). Optimal sleep modified both cognitive performance and dementia risk in individuals with focal epilepsy compared with stroke patients and healthy controls. 2 key findings →

Design: cohort study Evidence: moderate

Symptomatic females with genetic FTD had lower frontal cortical thickness than males, and the C9orf72 subgroup showed lower-than-expected frontal cortical thickness for a given level of executive functioning. 5 key findings →

Design: longitudinal study Participants: 394 Evidence: moderate

Self- and Informant-Report Cognitive Decline Discordance and Mild Cognitive Impairment Diagnosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. JAMA Network Open 2025-04-18

ADNI participants (921 dyads) had a mean (SD) age of 71 (7) years and mean (SD) of 17 (3) years of education; 485 (53%) were female, 30 (3%) were Asian, 105 (11%) were Black, and 756 (82%) were White. eVAL participants (279 dyads) had a mean (SD) age of 71 (8) years and mean (SD) of 17 (2) years of education; 151 (54%) were female, 17 (6%) were Asian, 12 (4%) were Black, and 245 (88%) were White. 5 key findings →

Design: cross-sectional Participants: 921 Evidence: moderate

A decreasing linear trend was observed between higher levels of curry consumption and cognitive decline (p = 0.037). 4 key findings →

Design: cohort study Participants: 2,920 Evidence: moderate

Outdoor activity is linked to lower dementia risk, particularly in those living in more accessible GS. 5 key findings →

Design: longitudinal study Participants: 187,724 Evidence: moderate

Neurodegenerative disorders such as Alzheimer's disease (AD), the most common form of dementia, represent a growing global health crisis, yet current treatment strategies remain primarily palliative. 2 key findings →

Design: longitudinal study Evidence: moderate

After the intervention, the CG showed significantly lower scores compared to all experimental groups. 4 key findings →

Design: randomized controlled trial Participants: 92 Evidence: high

Combining aerobic exercise with cognitive training improves clinical outcomes in older adults with MCI and may influence stress-related neurobiological pathways. 5 key findings →

Design: randomized controlled trial Participants: 28 Evidence: high

Among the five personality domains, only extraversion was significantly associated with reduced odds of cognitive decline within the intervention group over 24 weeks (fully adjusted model: OR = 0.35; 95% CI: 0.15-0.82). 2 key findings →

Design: randomized controlled trial Participants: 136 Evidence: high

Cerebral small vessel disease (SVD) is recognized as a major vascular contributor to cognitive decline, ultimately leading to dementia and stroke. 1 key finding →

Design: longitudinal study Evidence: moderate

Sensitivity analyses were performed to validate the robustness of the linear regression results. 4 key findings →

Design: longitudinal study Participants: 832 Evidence: moderate

Lecanemab was approved for early Alzheimer's disease in Japan, with ≈ 6000 patients treated in the first year post approval. 2 key findings →

Participants: 6,000 Evidence: low

The advent of anti-amyloid monoclonal antibody (mAb) therapies represents a paradigm shift in the treatment of Alzheimer's disease (AD), from symptomatic relief to disease modification. 5 key findings →

Design: randomized controlled trial Evidence: high

Residents' QoL was negatively associated with advanced dementia, PDU, and NPS. 5 key findings →

Design: cross-sectional Participants: 207 Evidence: low

Of 4,150 studies screened, 26 were eligible for inclusion, of which 17 were human studies, 8 were preclinical animal studies, and 1 included both human and preclinical animal studies. 4 key findings →

Design: narrative review Participants: 12 Evidence: low

The potential neuroprotective effects of antidiabetic treatments have been largely assessed in Alzheimer's disease (AD) and AD-like dementia models, with or without metabolic disorders. 1 key finding →

Design: systematic review Participants: 405 Evidence: low

↑ 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.

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