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.

These findings suggest that a hearing intervention might reduce cognitive change over 3 years in populations of older adults at increased risk for cognitive decline but not in populations at decreased risk for cognitive decline. 5 key findings →

Design: randomized controlled trial Participants: 858 Evidence: high

Association Between Midlife Vascular Risk Factors and Estimated Brain Amyloid Deposition

✓ Peer-reviewed alzhub usefulness score 75 out of 100. JAMA 2017-04-01

An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR; this association was not significant for late-life risk factors. 5 key findings →

Design: cohort study Participants: 20 Evidence: moderate

Over a long period of observation, no evidence was found that a specific AHM drug class was more effective than others in lowering risk of dementia. 4 key findings →

Design: meta-analysis Participants: 31 Evidence: high

In this study, risk of dementia significantly increased after ischemic stroke, independent of vascular risk factors. 5 key findings →

Design: prospective cohort Participants: 379 Evidence: moderate

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

Cerebral small vessel disease genomics and its implications across the lifespan

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Nature communications 2020-12-08

White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →

Evidence: moderate

Vascular factors predict rate of progression in Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Neurology 2007-11-01

Atrial fibrillation, hypertension, and angina were associated with a greater rate of decline and may represent modifiable risk factors for secondary prevention in Alzheimer disease. 3 key findings →

Design: longitudinal study Participants: 135 Evidence: moderate

We tested whether dysregulation of cholesterol catabolism, through its conversion to primary bile acids (BAs), was associated with dementia pathogenesis. 5 key findings →

Design: cohort study Participants: 141 Evidence: moderate

Head injury and 25-year risk of dementia

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2021-03-09

Head injury was associated with risk of dementia (hazard ratio [HR] = 1.44, 95% confidence interval [CI] = 1.3-1.57), with evidence of dose-response (1 head injury: HR = 1.25, 95% CI = 1.13-1.39, 2+ head injuries: HR = 2.14, 95% CI = 1.86-2.46). 3 key findings →

Design: cohort study Participants: 14,376 Evidence: moderate

From October 2018 to March 2020, 58 participants were recruited (29 per group, 95% [86%-99%]). 5 key findings →

Design: randomized controlled trial Participants: 58 Evidence: high

Stroke, dementia, and hypertension are associated with late-onset epilepsy; however, the role of other vascular and lifestyle factors remains unclear. 5 key findings →

Design: cohort study Participants: 792 Evidence: moderate

Risk Factors Associated With Late-Onset Epilepsy in Dementia and Mild Cognitive Impairment

✓ Peer-reviewed alzhub usefulness score 65 out of 100. JAMA Neurology 2025-04-14

Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. 5 key findings →

Design: longitudinal study Participants: 713 Evidence: moderate

= 0.009). Significant differences in annualized changes in these FA and MD values were found depending on the presence or absence of type 2 diabetes and smoking. 4 key findings →

Design: longitudinal study Participants: 6,471 Evidence: moderate

More-severe diabetes (defined by higher HbA 1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. 3 key findings →

Design: cross-sectional Participants: 1,713 Evidence: low

Growing evidence suggests that fine particulate matter (PM 2.5 ) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. 5 key findings →

Design: cohort study Evidence: moderate

An AI-Powered Lifestyle Intervention vs Human Coaching in the Diabetes Prevention Program

✓ Peer-reviewed alzhub usefulness score 64 out of 100. JAMA 2025-10-27

A total of 368 participants were included (median [IQR] age, 58 [50-65] years; 71% were female, 27% were Black, 6% were Hispanic, and 61% were White; median [IQR] BMI, 32.3 [28.5-37.1]). 5 key findings →

Design: clinical trial Participants: 368 Evidence: high

Diabetes status, poor glycemic control, and longer diabetes duration were associated with worse cognitive outcomes over a median follow-up of 5 years. 4 key findings →

Participants: 5,099 Evidence: low

Studies of long-term cognitive change should account for the potential effects of education on the outcome, since some studies have demonstrated an association of education with dementia risk. 4 key findings →

Design: cohort study Participants: 14,020 Evidence: moderate

Large-scale plasma proteomic analysis identifies proteins and pathways associated with dementia risk

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Nature aging 2021-05-14

The plasma proteomic changes that precede the onset of dementia could yield insights into disease biology and highlight new biomarkers and avenues for intervention. 4 key findings →

Participants: 4,110 Evidence: moderate

Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized. 1 key finding →

Design: cohort study Participants: 37,096 Evidence: moderate

Differences between users and non-users of insulin, metformin and sulfonylurea were assessed in each cohort for cognitive and brain MRI measures using linear regression models, and cognitive decline and dementia/AD risk using mixed effect models and Cox regression analyses, respectively. 4 key findings →

Participants: 3,590 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,040 records (3.4% of the library) are not peer-reviewed — 965 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    Where this research is being discussed: events