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 purpose of this meta-analysis was to determine the common signature of dysregulated brain glucose metabolism in late-onset age-associated neurodegenerative diseases (A2NDs), including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis. 2 key findings →

Design: meta-analysis Participants: 5,298 Evidence: high

Serum Brain-Derived Neurotrophic Factor Across the Human Lifespan: A Systematic Review and Meta-Analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-14

BackgroundBone marrow megakaryocytes, the primary source of brain-derived neurotrophic factor (BDNF) in the blood, secrete BDNF-packed platelets into the bloodstream. 3 key findings →

Design: meta-analysis 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⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Artificial intelligence can assist providers in a variety of patient care and intelligent health systems. 1 key finding →

Design: meta-analysis Evidence: high

To better characterize the genetic architecture underlying Alzheimer's disease (AD) and related dementia (ADRD), we performed a meta-analysis of European ancestry genome-wide association studies in 128,681 cases or proxy cases of ADRD and 849,833 (proxy) controls. 3 key findings →

Design: meta-analysis Evidence: high

Genetic drivers of progression in Alzheimer's disease are distinct from disease risk

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2025-11-19

Established AD risk factors, including APOE ε4 dosage and polygenic risk scores, were not associated with disease progression amyloid positive individuals who are actively declining. 5 key findings →

Design: meta-analysis Participants: 222 Evidence: high

Pervasive biases in proxy GWAS based on parental history of Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2023-10-17

Almost every recent Alzheimer's disease (AD) genome-wide association study (GWAS) has performed meta-analysis to combine studies with clinical diagnosis of AD with studies that use proxy phenotypes based on parental disease history. 2 key findings →

Design: meta-analysis Evidence: high

APOE Genotype and Fluid Biomarkers of Blood-Brain Barrier Integrity: A Systematic Review and Meta-Analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-09-29

Apolipoprotein E (APOE) genotype is theorised to influence dementia risk partly through effects on blood–brain barrier (BBB) function, but clinical studies examining APOE effects on BBB biomarkers report inconsistent results. 5 key findings →

Design: systematic review Participants: 5,375 Evidence: high

The Edinburgh Cognitive and Behavioral ALS Screen (ECAS) is the most validated and widely-used ALS-specific cognitive assessment tool, yet paper-and-pencil manual scoring introduces inter-rater variability that can significantly limit reliability and reproducibility in multi-site clinical trials. 2 key findings →

Design: meta-analysis Evidence: high

Genetic susceptibility to Lewy body disease and the distribution of Lewy pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-24

Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant. 4 key findings →

Design: meta-analysis Participants: 1,362 Evidence: high

Integration of cell-specific gene expression and chromatin accessibility facilitates localization of neurodegenerative risk in microglia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-17

Genome-wide association studies (GWAS) have identified many loci that contribute to the risk of neurodegenerative diseases. 3 key findings →

Design: meta-analysis Evidence: high

Effectiveness of Modern Diagnostic and Therapeutic Interventions for Major Neurological Disorders: A Systematic Literature Review

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-12

From 464 identified records, 30 peer-reviewed primary studies met all eligibility criteria following the exclusion of low-quality sources and unindexed preprints. 3 key findings →

Design: meta-analysis Evidence: high

Simulation-based validation demonstrates the framework’s analytical capability. 5 key findings →

Design: systematic review Evidence: high

SGLT2 inhibitors and GLP-1 receptor agonists have the greatest effect on cognition in T2DM, and the multi-component exercise as the most effective lifestyle component. 3 key findings →

Design: meta-analysis Participants: 213,604 Evidence: high

Eligible studies reported MACE or dementia outcomes in adults ≥ 50 years for at least one of three intervention classes (RZV, SGLT2i, GLP-1 RA) versus placebo or active comparator, with follow-up ≥ 6 months. 5 key findings →

Design: systematic review Evidence: high

Multidomain lifestyle interventions for the risk reduction of cognitive impairment and dementia: A systematic review and meta-analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-15

Multidomain interventions have small but consistent beneficial effects on cognitive measures, suggesting the potential to reduce cognitive impairment and dementia risk. 3 key findings →

Design: systematic review Participants: 23,209 Evidence: high

In brain, inverse-variance random-effects meta-analysis (DerSimonian–Laird) across six independent postmortem adult-brain GEO cohorts (GSE33000, GSE132903, GSE173955, GSE159699, GSE5281, GSE48350) yielded 458 analyzable panel genes, 167 at Benjamini–Hochberg FDR < 0.05, and 141 high-confidence genes (FDR < 0.05, measured in at least three cohorts, direction-concordant in at least 70% of cohorts, and nominally significant in at least two cohorts). 1 key finding →

Design: meta-analysis Participants: 329 Evidence: high

The ability to decode others’ emotions from multisensory cues is central to social functioning. 3 key findings →

Design: systematic review Participants: 1,511 Evidence: high

Panel-Gene Transcriptomic Associations and Published-Variant Architecture in Parkinson Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-22

Parkinson disease (PD) was examined in four primary adult-brain GEO cohorts (GSE49036, GSE20141, GSE8397, GSE7621) using a frozen 468-gene redox, metal, xenobiotic, and barrier panel. 1 key finding →

Design: meta-analysis Evidence: high

Environmental Exposures and Brain Health Outcomes in Healthy Ageing: A Systematic Review

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. PsyArXiv 2026-08-27

Of 2,496 records screened, 26 studies met eligibility, comprising >84,000 older adults across 10 countries: United States, South Korea, United Kingdom, France, Spain, Sweden, Netherlands, Taiwan, Germany, and Japan. 4 key findings →

Design: systematic review Evidence: high

Neuroinflammation is a hallmark of Alzheimer’s disease (AD); however, which neuroinflammatory effectors are consistently altered across independent human cohorts, brain regions, and microglial states—and can be engaged by available compounds—remains incompletely defined. 4 key findings →

Design: meta-analysis 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