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.

The critical role of primary care clinicians (PCCs) in Alzheimer's disease (AD) prevention, diagnosis and management must evolve as new treatment paradigms and disease-modifying therapies (DMTs) emerge. 4 key findings →

Evidence: low

Fit of the models to the data was adequate for general cognitive performance (root mean squared error of approximation (RMSEA)=0.03; comparative fit index (CFI)=0.94; standardised root mean residual (SRMR)=0.05), language (RMSEA=0.02; CFI=0.95; SRMR=0.05) and good for memory (RMSEA=0.05; CFI=0.99; SRMR=0.02) and executive functioning (RMSEA=0.03; CFI=0.98; SRMR=0.03). 5 key findings →

Design: cohort study Participants: 5,878 Evidence: moderate

PLWD also commonly experience social isolation (Shen et al., 2022), poorer physical function (Jehu et al., 2024a), worsened behavioral and psychological symptoms (Cerejeira et al., 2012), poorer quality of life (Cerejeira et al., 2012), and reduced access to healthcare (Mitchell et al., 2016) compared to older adults without dementia. 5 key findings →

Design: randomized controlled trial Participants: 21 Evidence: high

AD patients with ELA expressed significantly greater levels of APOE than ALA APOE ε4 carriers. 3 key findings →

Participants: 60,908 Evidence: low

Under Bronfenbrenner's macrosystem framework, we highlight key quantitative and qualitative studies linking S/SDOH with AD/ADRD, identify scientific gaps in the literature, and propose guidance for future research. 1 key finding →

Evidence: low

Identification of potentially modifiable risk factors for cognitive deterioration is important. 5 key findings →

Participants: 5,607 Evidence: low

This study tested the hypotheses that late-midlife obstructive sleep apnea (OSA) and short and long sleep duration are associated with dementia over 15 years of follow-up. 4 key findings →

Participants: 1,667 Evidence: low

Collectively, plasma biomarker findings in the low p-tau217 subgroup were more robust than in the mITT population. 5 key findings →

Design: clinical trial Evidence: high

Simulated Electroconvulsive Therapy: A Novel Approach to a Control Group in Clinical Trials

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The journal of ECT 2022-03-01

Validation of the safety and efficacy of ECT in patients with advanced AD with refractory agitation and aggression is necessary. 5 key findings →

Design: randomized controlled trial Evidence: high

Loss-of-function mutations in the GBA gene are associated with more severe cognitive impairment in PD, but the nature of these deficits is not well understood and whether common GBA polymorphisms influence cognitive performance in PD is not yet known. 4 key findings →

Participants: 60 Evidence: low

The rural setting presented unique challenges including: low literacy rates (60.1% of participants had no schooling), diverse language use (primarily Giriama and Swahili), limited infrastructure (e.g., 44.8% of households had electricity), restrictive cultural norms that influenced data collection (e.g., in-home interviews were often conducted outdoors with destructions). 5 key findings →

Design: longitudinal study Participants: 202 Evidence: moderate

AF is associated with greater cognitive decline and increased risk of dementia, independent of ischemic stroke. 5 key findings →

Participants: 515 Evidence: low

Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life. 3 key findings →

Participants: 229 Evidence: moderate

We studied the frequency, severity, and clinical correlations of cerebral amyloid angiopathy (CAA) in 117 CERAD subjects with autopsy-confirmed AD. 4 key findings →

Evidence: low

Forty-three proteins were differentially regulated in FTD compared to controls and AD, reflecting axon development, regulation of synapse assembly, and cell-cell adhesion mediator activity pathways. 5 key findings →

Participants: 189 Evidence: moderate

Early detection of Alzheimer's disease (AD) is critical yet challenging, particularly in younger individuals. 1 key finding →

Design: longitudinal study Participants: 120 Evidence: moderate

These results suggest that emerging biomarkers in conjunction with core AD markers improve diagnosis of AD, are associated with the conversion from MCI into AD, and predict a faster progression of dementia. 3 key findings →

Design: longitudinal study Participants: 319 Evidence: moderate

↑ 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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    Where this research is being discussed: events