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.

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⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

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⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Returning APOE and pTau-217 Results: the eSMARTER Randomized Noninferiority Clinical Trial

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-01

ImportancePatients are increasingly learning Alzheimers disease (AD) genetic and biomarker results through electronic health portals. 5 key findings →

Participants: 216 Evidence: high

Causal roles of phenotypic age and metabolic health on dementia: a Mendelian randomisation and structure learning study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

BackgroundPhenotypic age acceleration (PhenoAgeAccel), derived from PhenoAge, and MetaboHealth are composite exposures of biological ageing and metabolic health associated with dementia-related outcomes. 4 key findings →

Design: longitudinal study Participants: 272 Evidence: moderate

Integrative multi-omics QTL colocalization maps regulatory architecture in aging human brain

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-04

Multi-trait QTL (xQTL) colocalization has shown great promises in identifying causal variants with shared genetic etiology across multiple molecular modalities, contexts, and complex diseases. 2 key findings →

Participants: 595 Evidence: low

INTRODUCTIONMultimodal biomarkers have transformed Alzheimers disease research, but the incremental contribution of each modality to predicting progression from mild cognitive impairment (MCI) remains unclear. 3 key findings →

Participants: 2,430 Evidence: low

BackgroundAccurate prediction of progression from mild cognitive impairment (MCI) to Alzheimers disease (AD) is important for prognosis, patient management, and clinical trial enrollment. 5 key findings →

Participants: 2,430 Evidence: low

Alzheimer's Polygenic Risk Scores Are Not Interchangeable: Evidence from 1,752 Models

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

IntroductionPolygenic risk scores (PRS) may improve Alzheimers disease (AD) risk prediction before symptom onset, yet choosing an appropriate model can be challenging. 1 key finding →

Evidence: low

Alzheimers disease (AD) is characterized by substantial clinical and biological heterogeneity, with diverse neuroanatomical, cognitive, clinical, functional, and genetic risk profiles that are poorly captured by current diagnostic frameworks. 4 key findings →

Participants: 393 Evidence: low

Sex differences in Alzheimers disease (AD) genetic effects and regulatory contexts remain incompletely resolved. 3 key findings →

Participants: 449,335 Evidence: low

ResultsThe CNR2 missense variant rs4649124 was associated with increased vascular dementia risk (BH-adjusted P = 0.049) after correction at the 5% false discovery rate (FDR) threshold, with additional associations at the 10% FDR threshold for all-cause dementia risk (BH-adjusted P = 0.051) and lower circulating APP (BH-adjusted P = 0.088) and BDNF (BH-adjusted P = 0.083) levels. 5 key findings →

Evidence: low

Multi-trait Polygenic Profiling and Survival Free of Dementia and Disability: Results from the Health and Retirement Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-11

ObjectiveTo determine whether a multi-trait polygenic profile for dementia is associated with dementia- and disability-free survival in middle-aged and older adults. 5 key findings →

Design: longitudinal study Evidence: moderate

Pathway-specific polygenic risk scores reveal underlying mechanisms of cerebral small vessel disease

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

White matter hyperintensities (WMH), a key MRI-marker of cerebral small vessel disease (cSVD), are common in older adults and associated with an increased risk of stroke and dementia. 5 key findings →

Participants: 46,944 Evidence: moderate

Alzheimers disease and related dementias (ADRD)1 and Parkinsons disease and related disorders (PDRD)2 have substantial genetic contributions, yet the role of rare damaging coding variants remains incompletely characterized at population scale3-6. 1 key finding →

Evidence: low

A longitudinal study of age-related traits and cognitive function: The Collaborative Amish Aging and Memory Project (CAAMP)

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-20

Structured AbstractO_ST_ABSINTRODUCTIONC_ST_ABSThe Collaborative Amish Aging and Memory Project (CAAMP) is an ongoing longitudinal study spanning multiple sites, focused on cognitive function and age-related traits in Midwestern Amish (Ohio and Indiana) communities. 5 key findings →

Design: prospective cohort Participants: 3,978 Evidence: moderate

Genetically Predicted Blood DNA Methylation Reveals Putative Regulatory Signals Associated with ALS Risk

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-20

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder whose genetic architecture and underlying molecular mechanisms remain incompletely understood, particularly in sporadic disease. 5 key findings →

Evidence: low

Associations of menopause hormone therapy with late-life cognition and brain health vary by formulation and APOEε4 presence

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-20

Implications of menopause hormone therapy (MHT) for cognitive aging remain unclear despite decades of research. 3 key findings →

Participants: 8,741 Evidence: low

INTRODUCTIONMultimodal lifestyle interventions can delay or slow Alzheimers disease (AD) in at-risk older adults, and plasma pTau217, a blood-based biomarker, now enables scalable AD risk stratification. 3 key findings →

Evidence: moderate

Genetic Associations with Alzheimer's, Lewy Body and Vascular Neuropathology Reveal Shared and Distinct Biological Pathways

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-22

INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia. 5 key findings →

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