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.

Tryptanthrin Analogs Substoichiometrically Inhibit Seeded and Unseeded Tau4RD Aggregation

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2024-02-03

Microtubule-associated protein tau is an intrinsically disordered protein (IDP) that forms characteristic fibrillar aggregates in several diseases, the most well-known of which is Alzheimer's disease (AD). 5 key findings →

Evidence: low

Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD). 4 key findings →

Design: clinical trial Evidence: low

Vasomechanic treatment increases efflux of human brain proteins

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-23

An age-related decline in vasodilation mediated by neurovascular nitric oxide (NO) and vasoconstriction driven by the Piezo1 receptor precede the aggregation of soluble brain proteins such as amyloid-β (Aβ), which then causes further disruption of brain solute homeostasis, ultimately leading to neurodegeneration in Alzheimer’s disease. 1 key finding →

Participants: 29 Evidence: low

CSF Alzheimer’s Disease Biomarkers in Relation to Functional Status and Tofersen Treatment Response in ALS

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-28

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease primarily affecting motor neurons but also frequently involving cognitive impairment. 4 key findings →

Design: longitudinal study Evidence: moderate

Living arrangements shape the determinants of life-sustaining treatment preferences among Korean older adults

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-31

Although most Korean older adults declined LST regardless of living arrangement, determinants of LST preferences differed according to household structure. 5 key findings →

Design: longitudinal study Participants: 3,787 Evidence: moderate

These integrated findings support H. erinaceus as a candidate adjunct to donepezil, with possible complementary effects on amyloidogenic processing and intracellular clearance. 3 key findings →

Evidence: low

Alzheimer’s disease (AD) is a progressively characterized neurodegenerative condition marked by molecular instability, neuronal dysfunction and abnormal tau buildup. 4 key findings →

Evidence: low

Integrated Transcriptomic and Structural Prioritization of Sulforaphane Targets in Neurodegeneration: A Multi-Dataset In Silico Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-25

Sulforaphane (SFN), a natural isothiocyanate from cruciferous vegetables, exerts neuroprotective effects through mechanisms extending beyond canonical Nrf2/ARE activation. 3 key findings →

Evidence: low

CausalDiffChem: Causal Network Restoration for Therapeutic Prioritization and Repurposing Across Diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-26

Computational drug repurposing commonly relies on transcriptomic signature matching to identify compounds that reverse disease-associated gene expression, but such approaches do not distinguish putative causal drivers from downstream consequences of disease. 1 key finding →

Evidence: low

: Treated patients were 74±7 years old; 57% were female, 59% were apolipoprotein E ε4 carriers, and 78% had mild cognitive impairment (22% mild dementia). 5 key findings →

Participants: 15 Evidence: low

Opposing Regulation of Tau Condensation by Phosphorylation Levels and Molecular Chaperone Interactions

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30

Aggregation of the microtubule-stabilizing protein Tau into insoluble deposits is characteristic for several neurodegenerative diseases, including Alzheimer's disease. 3 key findings →

Evidence: low

Alzheimer's Disease (AD), the most common neurodegenerative disease in the world, is caused by a variety of factors that lead to neuronal injury and an alteration in neurotransmitter production and release. 2 key findings →

Evidence: low

Brain-resident myeloid cells promote rapid leukocyte adhesion in leptomeningeal vessels after anti-Aβ immunotherapy

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-11

Anti-amyloid-β (Aβ) immunotherapy improves cognitive outcomes in Alzheimer’s disease (AD) but is associated with amyloid-related imaging abnormalities (ARIA), through poorly understood mechanisms. 3 key findings →

Design: longitudinal study Evidence: moderate

CSF Aβ42 rose from 526.0 to 1053.0 pg/mL (+ 100.2%), total tau (t-tau) fell from 578.2 to 278.0 pg/mL(-51.9%), and phosphorylated tau181 (p-tau181) fell from 90.8 to 23.1 pg/mL(-74.6%). 2 key findings →

Evidence: low

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

Amyloid plaques, one of the defining features of Alzheimer’s disease, are associated with synapse loss and accumulation of pathological tau in dystrophic neurites and reactive glia in their immediate vicinity. 3 key findings →

Evidence: low

Artificial Intelligence in Alzheimer’s Disease: Evidence Maturity and Clinical Translation Across the Care Pathway

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-07-30

Artificial intelligence (AI) is now a credible translational research platform across the Alzheimer’s disease (AD) pathway, but its clinical value is often difficult to judge from performance metrics alone. 5 key findings →

Design: longitudinal study Evidence: moderate

A major obstacle to effective Alzheimer’s disease therapy is the limited ability to deliver therapeutics across the blood-brain barrier. 2 key findings →

Evidence: low

From across this tag

10 of the 3,541 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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