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.

Genomics link obesity and type 2 diabetes to Alzheimers disease to unveil novel biological insights

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →

Evidence: low

MRI-derived brain aging trajectories across the Alzheimer's continuum: links to cognition, pathology and lifestyle risk factors

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-22

BackgroundThe brain age gap (BAG), the difference between neuroimaging-predicted and chronological age, captures inter-individual variation in brain aging. 2 key findings →

Design: longitudinal study Participants: 202 Evidence: moderate

AbstractO_ST_ABSBackgroundC_ST_ABSGlucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used for type 2 diabetes. 5 key findings →

Participants: 6,328 Evidence: low

In the fully adjusted Cox model, baseline statin exposure was associated with a lower risk of incident AMI (HR, 0.805; 95% CI, 0.731-0.887). 3 key findings →

Design: cohort study Participants: 174,014 Evidence: high

Persistent racial disparities in dementia raise concerns regarding the validity and generalizability of existing prognostic models across diverse populations. 2 key findings →

Participants: 55,004 Evidence: moderate

BACKGROUNDPeople with type 2 diabetes mellitus (T2DM) are at higher risk of cerebral small vessel disease and left ventricular hypertrophy (LVH), potentially contributing to cognitive decline and dementia. 5 key findings →

Design: cohort study Participants: 62 Evidence: moderate

Cerebral Small Vessel Disease and Risk of Cardiovascular Events and All-Cause Mortality: The Framingham Heart Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-07

O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/26361997v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1dac0d9org.highwire.dtl.DTLVardef@aaf8f2org.highwire.dtl.DTLVardef@be10a1org.highwire.dtl.DTLVardef@35c7be_HPS_FORMAT_FIGEXP M_FIG C_FIG BACKGROUNDThe effect of neurovascular health on cardiovascular outcomes is not well-known. 4 key findings →

Participants: 3,263 Evidence: moderate

Cognition in Whitehall II 'SuperAgers': An Analysis of Dementia Risk Factors

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

Higher education (OR = 1.23, SE = 0.05, 95% CI = [1.10, 1.36], p < 0.001), female sex (OR = 1.30, SE = 0.09, 95% CI = [1.10, 1.55], p = 0.003), and lower age (OR = 0.67, SE = 0.04, 95% CI = [0.61, 0.73], p < 0.001) were associated with increased odds of SuperAger status. 5 key findings →

Participants: 3,513 Evidence: moderate

Accelerometer-Derived Relative Amplitude and Midlife Cognition: A Cross-Sectional Study

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

ImportanceLower relative amplitude of the rest-activity pattern has been associated with cognitive decline and incident dementia in older adults, but its relationship with domain-specific cognitive performance during midlife is less well characterized. 5 key findings →

Design: cross-sectional Participants: 851 Evidence: moderate

Over a median follow-up of 13 years, 5,304 participants developed dementia. 4 key findings →

Participants: 151,832 Evidence: low

Public awareness of the hearing loss-dementia link and self-reported behavioral changes in middle- to older-aged Canadians

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-26

Hearing loss is a potential risk factor for dementia, but public awareness of this link and its behavioral implications remain poorly understood. 2 key findings →

Design: cross-sectional Evidence: low

The exposome factors, such as diet, lifestyle, microbiome, chemical exposures and social exposome, shapes human health beyond genetic influences, but the mechanisms remain only partially understood. 1 key finding →

Participants: 449 Evidence: low

Alzheimer disease,* the most common cause of dementia, affects an estimated 6.5 million persons aged ≥65 years in the United States (1). 2 key findings →

Evidence: low

Living in locations with higher PM2.5 (per interquartile range [IQR]=3.17μg/m3) or NO2 (per IQR=6.63ppb) was associated with greater MTL atrophy (βPM2.5 = -0.29, 95% confidence interval [CI]=[-0.41,-0.18]; βNO2 =-0.12, 95%CI=[-0.23,-0.02]). 5 key findings →

Design: longitudinal study Participants: 627 Evidence: moderate

Racial and Ethnic Differences in Subjective Cognitive Decline - United States, 2015-2020

⚠ Report — not peer-reviewed alzhub usefulness score 16 out of 100. MMWR. Morbidity and mortality weekly report 2023-03-10

Subjective cognitive decline (SCD), the self-reported experience of worsening or more frequent memory loss or confusion, might be a symptom of early-stage dementia or future serious cognitive decline such as Alzheimer disease* or a related dementia (ADRD) (1). 1 key finding →

Evidence: low

Cognition in healthy aging, ages 36 to 108: Associations with dementia risk factors and neurodegenerative disease biomarkers

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

Most evidence on dementia risk factors comes from older or clinical samples, leaving their relation to normal cognitive aging unclear. 4 key findings →

Participants: 1,396 Evidence: moderate

Multimodal mediators connecting APOE4 to dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-21

We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints. 5 key findings →

Participants: 58,876 Evidence: low

Plasma metabolomic profiling of frailty in older adults at risk of dementia

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

Frailty index was associated with carboxylic acids and derivatives, fatty acyls and organooxygen compounds across multiple clusters, and a large number of lipids were linked to frailty score, potentially implicating dysregulation of energy metabolism in the pathophysiology of frailty and forming a panel of predictive biomarkers of at risk patients. 3 key findings →

Participants: 118 Evidence: low

A sphingomyelin-cholesterol complex regulates TLR4 activation in microglia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14

Microglial activation in response to lipopolysaccharide (LPS) requires Toll-like receptor 4 (TLR4) redistribution into cholesterol- and sphingolipid-rich membrane domains, yet the lipid determinants of this process remain unclear. 1 key finding →

Evidence: low

Temporal Proteomics Links the APP London Mutation to Early Cholesterol Remodeling Cell Programs in Human Neurons

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

Familial Alzheimer’s disease (AD) mutations in amyloid precursor protein (APP) alter amyloid-β (Aβ) secretion profiles, but their effects on neuronal protein and lipid homeostasis remain incompletely understood. 4 key findings →

Design: longitudinal study Evidence: moderate

Closed-head injury produces a delayed, region-specific defect in glucose-carbon routing at the pyruvate branchpoint in APP/PS1 KI mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-06

Traumatic brain injury (TBI) is a risk factor for Alzheimer’s disease (AD), and both conditions are associated with impaired glucose metabolism and mitochondrial dysfunction. 2 key findings →

Evidence: low

Parental history of dementia is a risk factor for Alzheimer’s disease, although the mechanisms underlying this association remain poorly understood. 5 key findings →

Evidence: low

From across this tag

10 of the 3,795 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.

1,038 records (3.6% of the library) are not peer-reviewed — 966 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