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.

Midlife and late-life risk factors contributed to 22.7% and 16.5% of total dementia cases, respectively. 5 key findings →

Design: meta-analysis Participants: 37,931 Evidence: high

Cognitive training involving speed of cognitive processing has the potential to delay the diagnosis of ADRD. 1 key finding →

Design: randomized controlled trial Participants: 2,021 Evidence: high

Plasma Phosphorylated Tau 217 and Incident Mild Cognitive Impairment and Dementia in Older Women

✓ Peer-reviewed alzhub usefulness score 69 out of 100. JAMA Network Open 2026-03-02

Among 2766 participants (mean [SD] age, 69.9 [3.8] years; 486 [17.9%] Black, 196 [7.1%] Hispanic, and 2007 [73.9%] White), 1311 developed the combined end point of MCI or dementia (849 participants with MCI and 752 participants with dementia). 5 key findings →

Design: cohort Participants: 2,766 Evidence: moderate

The APOE-ε4/ε4 genotype is the strongest genetic risk factor for sporadic Alzheimer's disease, though the relative risk is diminished in individuals with African ancestry. 2 key findings →

Design: case-control Evidence: moderate

Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →

Design: cohort Evidence: high

The study included 1,028 participants (mean age at baseline 76.4 years; 47.6% female): 521 with ADP, 96 with LBP, and 411 with mixed AD-LBP. 5 key findings →

Design: cohort study Participants: 1,028 Evidence: moderate

Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. JAMA network open 2026-07-01

In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →

Design: case-control study Participants: 231 Evidence: moderate

A total of 30 variants were overrepresented in four pathways: presenilin/Alzheimer disease, cadherin/WNT signaling, gonadotropin-releasing hormone receptor, and transforming growth factor-β (TGF-β) signaling. 5 key findings →

Participants: 204 Evidence: low

Polygenic Risk Scores for Incident Dementia in the Multi‐Ethnic Study of Atherosclerosis

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Genetic Epidemiology 2026-06-23

We found comparable associations between dementia and PRS when comparing a C+T method with only 15 SNPs and PRS derived from Bayesian models that include > 800,000 SNPs (HR 5e‐08 = 1.18, 95% CI: 1.08–1.28; HR CSx = 1.17, 95% CI: 1.07−1.27). 3 key findings →

Evidence: low

Non-White race and adverse social and socioeconomic factors-lower education, unemployment, unmarried status, and greater neighborhood disadvantage-were each associated with poorer cognitive performance (p < 0.05). 4 key findings →

Participants: 274 Evidence: low

A total of 51 patients with AD, age (median: 73 years) and 53 cognitively normal subjects (median age: 69) were included. 5 key findings →

Participants: 51 Evidence: low

Identity-by-descent (IBD) mapping provides complementary signals to genome-wide association studies (GWASs) when multiple causal haplotypes or variants are present but not directly tested. 5 key findings →

Evidence: low

Compared to those in rural areas, participants who resided in urban areas during young adulthood had lower late midlife ADI (β = -0.85, p < .05), and better executive function (β = 0.19), processing speed (β = 0.24), and verbal fluency (β = 0.30) (ps < .05) in older adulthood. 4 key findings →

Evidence: low

In 2023, US life expectancy reached 78.5 years and healthy life expectancy 64.5 years, both still below prepandemic 2019 levels, with a persistent 13-14-year gap between life expectancy and healthy life expectancy. 5 key findings →

Evidence: low

BackgroundNeighborhood disadvantage has been associated with reduced cognitive reserve, increased risk for cognitive impairment, and greater Alzheimer's disease (AD) neuropathology, with particularly pronounced effects among Black and Hispanic/Latino older adults. 4 key findings →

Evidence: low

Abnormalities in core AD biomarkers precede inflammatory and glial markers in CSF in Autosomal Dominant Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-04-01

Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →

Participants: 484 Evidence: low

Plasma inflammatory biomarker associations with Alzheimers disease clinical stage and CSF biomarkers: evaluation of sex effects

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-17

BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses. 4 key findings →

Design: cross-sectional Participants: 261 Evidence: moderate

Conditional polygenic enrichment distinguishes causal from tagging disease-critical cell populations in single-cell RNA-seq

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-23

Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex. 3 key findings →

Evidence: low

BackgroundUp to 30% of individuals harboring core Alzheimers disease (AD) neuropathology--amyloid-{beta} (A{beta};A) and tau (T)--remain cognitively unimpaired. 1 key finding →

Design: cohort study Participants: 500 Evidence: moderate

Proteoform-resolved neoGFAP as a diagnostic and prognostic biomarker across the TBI--MCI--AD continuum in Veterans

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-03

Service members with traumatic brain injury are at approximately two- to four-fold higher risk of Alzheimers disease or related dementias than those without such an injury, with risk increasing with injury severity. 5 key findings →

Participants: 57 Evidence: moderate

These findings show that model-based, adaptive assessments can support high-frequency, remote detection and scalable longitudinal monitoring of early memory decline, providing a new way to assess memory decline trajectories in healthy aging and dementia. 3 key findings →

Design: longitudinal study Participants: 24 Evidence: moderate

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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