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.

SGLT2 Inhibitor Use and Risk of Dementia and Parkinson Disease Among Patients With Type 2 Diabetes

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Neurology 2024-09-18

In this nationwide population-based study, SGLT2i use significantly reduced the risks of neurodegenerative disorders in patients with type 2 diabetes independent of various factors including comorbidities and bioclinical parameters. 5 key findings →

Design: cohort Participants: 358,862 Evidence: moderate

Hearing Loss, Hearing Aid Use, and Risk of Dementia in Older Adults

✓ Peer-reviewed alzhub usefulness score 70 out of 100. JAMA Otolaryngology-Head & Neck Surgery 2024-02-01

The results of this cohort study suggest that hearing loss was associated with increased dementia risk, especially among people not using hearing aids, suggesting that hearing aids might prevent or delay the onset and progression of dementia. 5 key findings →

Design: cohort Participants: 573,088 Evidence: moderate

At 6 months, compared with usual care, participants receiving the intervention had better QOL (QOL-AD score, 0.09 [95% CI, -0.63 to 0.82] vs -0.88 [95% CI, -1.62 to -0.13]; treatment effect estimate, 0.97; 95% CI, 0.07-1.86; P = .03). 4 key findings →

Participants: 612 Evidence: high

In this 3-year randomized clinical trial, ω-3 treatment was safe and well-tolerated but failed to reach significant reductions in WML accumulation or neuronal integrity breakdown among all participants, which may be attributable to sample size limitations. 5 key findings →

Participants: 102 Evidence: high

In the discovery cohort, the mean (SD) age was 70.9 (8.5) years, 191 (58%) were male, the mean (SD) MMSE score was 27.1 (1.9), and 110 individuals with MCI (33%) converted to dementia (71 to AD dementia). 4 key findings →

Design: cohort study Participants: 110 Evidence: moderate

Brain clocks, which quantify discrepancies between brain age and chronological age, hold promise for understanding brain health and disease. 4 key findings →

Participants: 5,306 Evidence: low

Higher WMH volume was associated with older age, lower CSF amyloid-β levels, hypertension, and smoking history (all p ≤ 0.001), as well as cognitive status (MCI, p < 0.001; dementia, p = 0.008), but not with CSF tau levels. 5 key findings →

Design: longitudinal study Participants: 1,803 Evidence: moderate

The CDR+NACC FTLD global score interacted with time on battery percentage such that participants with prodromal or symptomatic FTLD demonstrated less change in battery percentage throughout the day (a proxy for less smartphone use) than clinically normal participants (P<.001 in both cases). 4 key findings →

Design: longitudinal study Participants: 94 Evidence: moderate

Genetic variants for Alzheimer's disease and comorbid conditions

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Journal of Alzheimer's disease : JAD 2024-11-10

Targeted analysis of 20 SNPs that were reported to be associated with ADRD revealed that six were significantly associated with dual-disease outcomes, specifically congestive heart failure and cancer. 4 key findings →

Design: longitudinal study Participants: 1,177 Evidence: moderate

Neuroimaging biomarkers and CSF sTREM2 levels in Alzheimer's disease: a longitudinal study

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Scientific reports 2024-07-03

Understanding the exact pathophysiological mechanisms underlying the involvement of triggering receptor expressed on myeloid cells 2 (TREM2) related microglia activation is crucial for the development of clinical trials targeting microglia activation at different stages of Alzheimer's disease (AD). 5 key findings →

Design: longitudinal study Participants: 1,001 Evidence: moderate

Participants with CIND displayed lower perfusion in the PCC+PCu relative to participants who were CN, but there was no statistically significant difference between the groups in amyloid burden in this region. 5 key findings →

Design: case-control study Participants: 113 Evidence: moderate

Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials. 2 key findings →

Design: cohort Participants: 795 Evidence: moderate

Disease staging of Alzheimer's disease using a CSF-based biomarker model

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Nature aging 2024-03-21

Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →

Design: longitudinal study Participants: 426 Evidence: moderate

APOE4 homozygozity represents a distinct genetic form of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Nature medicine 2024-05-06

This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD. 2 key findings →

Participants: 3,297 Evidence: low

Core CSF Biomarker Profile in Cerebral Amyloid Angiopathy: Updated Meta-Analysis

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Neurology 2024-09-13

There is a clear need to characterize and validate molecular biomarkers of cerebral amyloid angiopathy (CAA), in an effort to improve diagnostics, especially in the context of patients with Alzheimer disease (AD) receiving immunotherapies (for whom underlying CAA is the driver of amyloid-related imaging abnormalities). 4 key findings →

Design: meta-analysis Participants: 289 Evidence: high

Peripheral GFAP and NfL as early biomarkers for dementia: longitudinal insights from the UK Biobank

✓ Peer-reviewed alzhub usefulness score 69 out of 100. BMC medicine 2024-05-13

Peripheral glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are sensitive markers of neuroinflammation and neuronal damage. 4 key findings →

Design: cohort study Participants: 48,542 Evidence: moderate

Many coronavirus disease 2019 (COVID-19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting "brain fog" and mild cognitive impairments even months after the acute phase of infection. 5 key findings →

Design: systematic review Participants: 19 Evidence: high

Biomarker Changes during 20 Years Preceding Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 69 out of 100. The New England journal of medicine 2024-02-01

In this study involving Chinese participants during the 20 years preceding clinical diagnosis of sporadic Alzheimer's disease, we observed the time courses of CSF biomarkers, the times before diagnosis at which they diverged from the biomarkers from a matched group of participants who remained cognitively normal, and the temporal order in which the biomarkers became abnormal. 2 key findings →

Design: case-control study Participants: 648 Evidence: moderate

Overall the study included 199 participants with iRBD, 20 hyposmic participants with available dopamine transporter single-photon emission computed tomography, 146 nonmanifest GBA1N409S gene carriers, 21 GBA1N409S gene carrier patients with PD, 50 patients with sporadic PD, and 140 healthy controls. 3 key findings →

Design: cross-sectional Participants: 170 Evidence: low

Alzheimer's disease, a progressive neurodegenerative pathology, is characterized by the accumulation of Amyloid-β plaques in the brain. 5 key findings →

Design: systematic review Evidence: high

Blood Biomarkers to Detect Alzheimer Disease in Primary Care and Secondary Care

✓ Peer-reviewed alzhub usefulness score 68 out of 100. JAMA 2024-10-15

This Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone. 3 key findings →

Design: cross-sectional Participants: 1,213 Evidence: high

This observational study analyzed electronic health records of about 1.09 million US patients with type 2 diabetes and found that those prescribed semaglutide (a GLP-1 diabetes/weight-loss drug) were substantially less likely to receive a first-time Alzheimer's diagnosis over 3 years than those on other diabetes medications. 3 key findings →

Design: cohort Participants: 1,090,000 Evidence: preliminary

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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