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.

With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →

Participants: 1,422 Evidence: moderate

In a large cohort of cognitively unimpaired individuals enrolled in a Phase 3 clinical trial and companion observational study, these findings confirm that higher baseline levels of amyloid and tau markers are associated with increased rates of cognitive decline and progression to functional impairment. 5 key findings →

Design: longitudinal study Participants: 583 Evidence: high

Fifty-one AD patients enrolled, mean age 73.5. 4 key findings →

Design: clinical trial Evidence: high

Diagnosis of Alzheimer's disease using plasma biomarkers adjusted to clinical probability

✓ Peer-reviewed alzhub usefulness score 74 out of 100. Nature aging 2024-11-12

Recently approved anti-amyloid immunotherapies for Alzheimer's disease (AD) require evidence of amyloid-β pathology from positron emission tomography (PET) or cerebrospinal fluid (CSF) before initiating treatment. 4 key findings →

Design: cohort study Participants: 6,896 Evidence: moderate

This study provides evidence that the effects of GLP-1 receptor agonists may extend beyond their known metabolic and cardioprotective benefits to include neuroprotection, associated with a decreased risk of developing various neurodegenerative disorders. 5 key findings →

Design: cohort study Participants: 102,935 Evidence: moderate

This meta-analysis pooled 14 studies of the Mini-Cog, a 3-minute memory-and-clock-drawing test doctors can give in a routine visit, to see how well it catches dementia. 5 key findings →

Design: meta-analysis Participants: 7,194 Evidence: moderate

Despite the relatively low risk reduction associated with higher adherence to MedDiet among elderly, it should be considered that this population is the most affected. 3 key findings →

Design: meta-analysis Participants: 65,955 Evidence: moderate

Between Feb 24, 2021, and March 5, 2023, 377 dyads were randomly assigned (1:1), 189 to usual treatment and 188 to intervention. 2 key findings →

Design: RCT Participants: 377 Evidence: high

Delirium and incident dementia in hospital patients in New South Wales, Australia: retrospective cohort study

✓ Peer-reviewed alzhub usefulness score 72 out of 100. BMJ 2024-03-27

The study findings suggest delirium was a strong risk factor for death and incident dementia among older adult patients. 3 key findings →

Design: cohort Participants: 110,422 Evidence: moderate

APOE3 Christchurch Heterozygosity and Autosomal Dominant Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 72 out of 100. New England Journal of Medicine 2024-06-20

Clinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease. 3 key findings →

Design: cohort Participants: 1,077 Evidence: moderate

In participants with early symptomatic AD, zagotenemab failed to achieve significant slowing of clinical disease progression compared with placebo. 5 key findings →

Design: clinical trial Participants: 360 Evidence: high

Blood Astrocyte Biomarkers in Alzheimer Disease: A Systematic Review and Meta-Analysis

✓ Peer-reviewed alzhub usefulness score 72 out of 100. Neurology 2024-07-10

We demonstrated significant elevations in blood GFAP and YKL-40 levels in patients on the AD continuum compared with CU individuals. 5 key findings →

Design: systematic review Participants: 3,366 Evidence: high

SNAP-25 and 14-3-3 zeta/delta also had the strongest associations with tau-PET, amyloid-β-PET and cortical thickness at baseline and were associated with longitudinal changes in these imaging biomarkers [β(standard error, SE) = -0.056(0.0006) to 0.058(0.005), P < 0.0001]. 3 key findings →

Design: longitudinal study Participants: 205 Evidence: moderate

Despite most monoclonal antibodies against Aβ in Alzheimer's failed to demonstrate efficacy, the newest antibodies showed statistically significant clinical effects. 3 key findings →

Design: systematic review Evidence: high

Alzheimer's disease, prevalent in individuals aged 60 and above, constitutes most dementia cases and significantly impairs memory and cognitive functions. 5 key findings →

Design: systematic review Evidence: high

Explainable artificial intelligence (XAI) has gained much interest in recent years for its ability to explain the complex decision-making process of machine learning (ML) and deep learning (DL) models. 1 key finding →

Design: systematic review Evidence: high

Serum GFAP levels correlate with astrocyte reactivity, post-mortem brain atrophy and neurofibrillary tangles

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Brain 2024-05-03

The main findings demonstrated an association between serum GFAP level and post-mortem tau pathology (β = 12.85; P < 0.001) that was independent of amyloid deposits (β = 13.23; P = 0.02). 5 key findings →

Design: cohort Participants: 139 Evidence: moderate

Participants receiving CDCM showed significantly fewer behavioral and psychological symptoms (adjusted mean difference [AMD] in NPI score, -10.26 [95% CI, -16.95 to -3.58]; P = .003; Cohen d, -0.78 [95% CI, -1.09 to -0.46]), better mental health (AMD in SF-12 Mental Component Summary score, 2.26 [95% CI, 0.31-4.21]; P = .02; Cohen d, 0.26 [95% CI, -0.11 to 0.51]), and lower caregiver burden (AMD in BIZA-D score, -0.59 [95% CI, -0.81 to -0.37]; P Conclusions and relevance In this secondary analysis of a cluster randomized clinical trial, CDCM was associated with improved patient, caregiver, and health system-relevant outcomes over 36 months beyond the intervention period. 3 key findings →

Design: RCT Participants: 428 Evidence: high

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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