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.

Alzheimer’s disease blood-based biomarkers in the Boston Latino Aging Study (BLAST): Associations with cognition and depressive symptoms

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-15

Distinct biomarker associations with cognitive and emotional functioning support further longitudinal evaluation of BBMs for risk characterization in Latino older adults and potential disease monitoring applications. 3 key findings →

Design: longitudinal study Participants: 122 Evidence: moderate

Blood Plasma Coenzyme Q 10 and P-Selectin Are Predictive Factors for Mild Cognitive Dysfunction in Elderly Women

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-13

Detection of the early phases of cognitive dysfunction is critical for identifying individuals at risk of neurodegeneration before irreversible damage occurs. 3 key findings →

Design: cross-sectional Evidence: moderate

Although endoplasmic reticulum (ER) stress and maladaptive unfolded protein response (UPR) are increasingly implicated in Alzheimer’s disease (AD), the influence of vitamin D (VitD) on these mechanisms remains unclear. 1 key finding →

Evidence: low

Interventions targeting lifestyle and health behaviors support cognition in older adults at risk of dementia. 5 key findings →

Participants: 1,260 Evidence: high

NOS1AP is a genetically validated driver of tau pathology in Alzheimer’s disease (AD), yet the NOS1AP-tau interaction itself has remained pharmacologically untargeted. 5 key findings →

Evidence: low

Cannabidiol for chronic neuroinflammation: clinical pharmacology and what an interpretable trial will require

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Authorea Preprints 2026-10-05

Public interest in cannabinoid medicines has outpaced the clinical pharmacology needed to judge product, dose and route. 5 key findings →

Design: narrative review Evidence: low

Plasma immune signatures associate with neurodegeneration in frontotemporal lobar degeneration

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

In exploratory full-cohort models, the multivariate CNS signature achieved an area under the curve of 0.93, compared with 0.82 for the multivariate inflammation signature. 4 key findings →

Design: case-control study Participants: 177 Evidence: moderate

SHED-Derived Exosomes Attenuate Alzheimer's Disease Pathology in iPSC-Derived Cerebral Organoid Model

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-29

SHED exosome treatment demonstrated genotype-specific efficacy, selectively reducing p181-tau levels and restoring the p181-tau/Aβ42 ratio in FAD lines while elevating the protective Aβ42/Aβ40 ratio across both FAD and SAD backgrounds. 5 key findings →

Evidence: low

Tau-PET subtype modifies the association between plasma p-tau217 and memory in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-09-28

Tau-PET subtype modified the p-tau217–memory association, suggesting that the cognitive implications of plasma p-tau217 may vary with tau topography. 4 key findings →

Design: cross-sectional Participants: 396 Evidence: moderate

White Matter Slow-4 fALFF as a Complementary Marker in the Multimodal Alzheimer’s Disease Biomarker Landscape

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-24

WM fALFF was significantly associated with GFAP (partial RZ = 5.35%), amyloid PET (partial RZ = 2.17%), tau PET (partial RZ = 3.52%), executive function (partial RZ = 2.61%), and mPACC (partial RZ = 3.53%). 4 key findings →

Participants: 108 Evidence: low

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

Design: clinical trial Evidence: low

Clinically Relevant Biomarkers of Alzheimer's Disease Are Associated with Age and Cortical Atrophy in Chimpanzees ( Pan troglodytes )

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-18

Chimpanzees share a number of age-related brain changes with humans, such as reductions in neurons and increases in neuropathology. 5 key findings →

Design: cross-sectional Evidence: moderate

Plasma Biomarker Profiles in a Colombian Cohort of Heterozygous APOE3-Christchurch Carriers

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-18

APOE3 Ch -associated resilience is measurably reflected in plasma biomarker trajectories, indicating attenuation of both neuroinflammatory and neurodegenerative processes. 3 key findings →

Design: cross-sectional Evidence: low

Concordance between p-tau217 and Aβ was high in the AD and MCI groups (observed agreement 90.0% in each), but overall agreement across Cohort II was modest (166/351, 47.3%; Cohen's κ = 0.117, 95% CI 0.029–0.204). 3 key findings →

Design: longitudinal study Participants: 918 Evidence: moderate

Social isolation, loneliness, and blood-based AD/ADRD biomarkers in a nationally-representative study of middle-aged and older adults

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-08-10

Social isolation was associated with elevated blood-based biomarkers of neuronal injury, with variation by patterns of exposure over time. 5 key findings →

Participants: 3,862 Evidence: low

Test-retest reliability of plasma biomarkers and digital cognitive metrics at clinically meaningful timescales

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-23

Test-retest reliability measures are essential for interpretation of meaningful effects over time for plasma and digital outcomes. 1 key finding →

Participants: 92 Evidence: moderate

Epigenetic Clock Trajectories and Brain Health in Midlife

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-18

Middle-aged adults with faster 15-year epigenetic aging trajectories demonstrated worse cognitive performance, whereas those with slower biological aging trajectories exhibited cognitive resilience and more favorable AD biomarker profiles. 5 key findings →

Participants: 2,833 Evidence: low

↑ 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