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.

Trisomy 21 (Down syndrome, DS) is the most common genetic cause of mental retardation, resulting from triplication of the whole or distal part of human chromosome 21. 2 key findings →

Evidence: low

Type 2 diabetes (T2D) and dementia frequently co-occur, yet the biological mechanisms underlying this comorbidity remain incompletely understood. 1 key finding →

Evidence: low

The ABC-DS cohort showed similar Aβ PET burden but had a lower prevalence of ApoE4 carriers, younger age at clinical diagnosis and autopsy, shorter PET-autopsy interval, smaller amygdala and hippocampal volumes, more advanced CERAD scores, and no atherosclerosis compared to ADRC cohort (Figure 1). 5 key findings →

Evidence: moderate

Identification of candidate serum protein biomarkers in Down's syndrome dementia

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Alzheimer s & Dementia 2025-12-01

MOLDI-MS identified eighty-five proteins represented by multiple tryptic peptides, twenty-five of which showed significant differences between DS and controls, confirmed by WB and ELISA analysis. 5 key findings →

Participants: 50 Evidence: low

Alzheimer's disease (AD) and frontotemporal dementia can often be diagnosed accurately with careful clinical history, cognitive testing, neurological examination, and structural brain MRI. 1 key finding →

Evidence: low

Clinical and population-based epidemiological studies report variation in the observed prevalence and incidence of dementia with Lewy bodies (DLB). 3 key findings →

Evidence: low

The behavioural and mental health needs of people with PWS result from the interactions between biological vulnerabilities associated with having PWS and living in a changing and demanding environment. 4 key findings →

Evidence: low

Life Stress and Dementia Risk in Adults with Down Syndrome

✓ Peer-reviewed alzhub usefulness score 30 out of 100. Innovation in Aging 2025-12-01

We found that a higher baseline sum of stress events was associated with greater risk of conversion from baseline stable cognition to mild cognitive impairment (MCI) or dementia at follow up, even when controlling for age, sex, premorbid level of intellectual disability, site, clinical latency between assessments, and the presence of anxiety or depression (odds ratio = 1.53, p = 0.021). 5 key findings →

Evidence: low

Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →

Design: longitudinal study Participants: 1,669 Evidence: moderate

Multi-dimensional attention framework for personalized Alzheimer’s disease progression prediction across sporadic and genetic risk cohorts

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-17

Alzheimer’s disease manifests through heterogeneous progression patterns across diverse populations, yet current predictive models fail to capture this complexity while maintaining clinical interpretability. 4 key findings →

Design: longitudinal study Participants: 1,669 Evidence: moderate

ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels. 5 key findings →

Evidence: low

One night of closed-loop auditory stimulation during sleep enhances memory consolidation in patients with Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-17

INTRODUCTIONSleep-dependent memory consolidation is impaired early in Alzheimers disease (AD). 2 key findings →

Participants: 37 Evidence: high

Integrated genomic meta-analysis identifies cell-type-specific signatures and targets in early Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-23

Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data. 5 key findings →

Design: systematic review Evidence: high

↑ 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