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.

BackgroundAlzheimers Disease and Related Dementias (ADRD) is a growing global public health challenge, and caregivers experience high rates of burden, unmet needs, and system failures. 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⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Enhancing Emergency Care for Persons Living with Dementia: Innovation and Age-friendly Approaches in Three Emergency Departments

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

KEY POINTSO_LIThis paper demonstrates the feasibility of implementing Geriatric ED programs with targeted support for people living with or at risk for dementia across three distinct health systems in San Francisco. 5 key findings →

Evidence: low

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

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

The feasibility criteria of >80% was met. 5 key findings →

Evidence: high

Detecting Self-Repairs from Spontaneous Speech with Prompt Ablation Across LLMs and Fine-Tuned Encoder

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-25

Self-repairs - in-utterance revisions in which a speaker abandons and reformulates their speech - are a promising interpretable marker for speech-based cognitive screening. 1 key finding →

Evidence: low

Metabolomic signatures of data-driven type 2 diabetes subtypes and their associations with dementia and stroke risk

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-25

We examined whether their metabolomic profiles also differed and whether subtype-related metabolic patterns were associated with dementia, stroke, and all-cause mortality. 5 key findings →

Participants: 7,671 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

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

Perceptions of non-invasive brain stimulation and barriers to it's clinical translation: a multi-stakeholder focus group study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-26

ObjectivesNon-invasive brain stimulation (NIBS) holds significant promise for treating neurological and neuropsychiatric conditions, yet translation into routine clinical practice remains limited. 1 key finding →

Participants: 33 Evidence: low

Discordance Between Genetic Ancestry and Self-Reported Race Impacts Inference of Neuropsychiatric Burden in Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-26

IntroductionNeuropsychiatric symptoms (NPS)--including aggression, psychosis, anxiety, apathy, and depression--affect up to 85% of individuals with Alzheimers disease (AD) and are among its most disabling and costly manifestations, accelerating cognitive and functional decline, institutionalization, mortality, and healthcare costs. 1 key finding →

Evidence: low

Multimodal Transformer Modeling of Rapamycin Treatment in Alzheimer's Disease via Random Forest Feature Filtering

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-26

Rapamycin, an FDA-approved inhibitor of the mammalian target of rapamycin (mTOR) pathway, has demonstrated promising anti-aging and neuroprotective effects. 4 key findings →

Participants: 23 Evidence: moderate

Aspirin and healthy longevity within racial and ethnic minoritized older adults in the United States

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-27

ImportanceThe ASPREE randomized trial found no overall benefit of low-dose aspirin for disability-free survival among older adults. 4 key findings →

Design: randomized controlled trial Evidence: high

Early identification of cognitive impairment remains challenging in settings where comprehensive cognitive and clinical assessments are not available. 1 key finding →

Evidence: low

Adult Vaccination History and Plasma Biomarker Signatures in the Asymptomatic PREVENT-AD Cohort

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-27

BackgroundEpidemiological studies increasingly associate several adult vaccinations with lower risk of Alzheimers disease (AD) and dementia, but the biological mechanisms underlying these observations remain unclear. 5 key findings →

Design: longitudinal study Participants: 192 Evidence: moderate

Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear. 2 key findings →

Participants: 6,053 Evidence: moderate

Neuropsychiatric symptoms (NPS) are increasingly recognized as critical components of the disease progression in Alzheimers disease (AD), yet their relationship with neurodegeneration remain poorly characterized. 2 key findings →

Participants: 1,756 Evidence: low

Absorption and Co-expression Modules Show Where Polygenic and Proteomic Risk Scores Diverge in Neurodegenerative Diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-27

Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease. 3 key findings →

Evidence: moderate

Genetic associations with EEG signatures in mild cognitive impairment: insights into Alzheimer's disease pathophysiology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-28

Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression. 5 key findings →

Evidence: low

Impairment in the comprehension of morphosyntactic and transitivity information does not feature in current diagnostic guidelines for primary progressive aphasia (PPA) or Alzheimers Diseases (AD), despite research reporting delayed sensitivity or insensitivity of these clinical populations to these linguistic domains. 2 key findings →

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