30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Midlife vascular risk factors are associated with increased risk of dementia in black and white ARIC Study participants. 4 key findings →
Design: prospective cohort Participants: 744 Evidence: moderate
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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
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Dementia is a significant public health challenge and may have greater incidence among older adults from underrepresented racial and ethnic minority groups. 4 key findings →
Design: cohort study Participants: 90 Evidence: moderate
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Among older patients with type 2 diabetes, a history of severe hypoglycemic episodes was associated with a greater risk of dementia. 5 key findings →
Design: cohort study Participants: 16,667 Evidence: moderate
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Exposure to several types of strong anticholinergic drugs is associated with an increased risk of dementia. 5 key findings →
Design: case-control study Participants: 769 Evidence: moderate
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MCR is common in older adults, and is a strong and early risk factor for cognitive decline. 3 key findings →
Design: cohort study Participants: 26,802 Evidence: moderate
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Despite the relatively low risk reduction associated with higher adherence to MedDiet among elderly, it should be considered that this population is the most affected. 3 key findings →
Design: meta-analysis Participants: 65,955 Evidence: moderate
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Higher adherence to a MedDiet was associated with lower dementia risk, independent of genetic risk, underlining the importance of diet in dementia prevention interventions. 3 key findings →
Design: cohort Participants: 60,298 Evidence: moderate
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In this cohort study of a Korean population, decreased risk of dementia was associated with maintaining mild to moderate alcohol consumption, reducing alcohol consumption from a heavy to a moderate level, and the initiation of mild alcohol consumption, suggesting that the threshold of alcohol consumption for dementia risk reduction is low. 5 key findings →
Design: cohort Participants: 3,933,382 Evidence: moderate
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Greater consumption of caffeinated coffee and tea was associated with lower risk of dementia and modestly better cognitive function, with the most pronounced association at moderate intake levels. 5 key findings →
Design: cohort Participants: 131,821 Evidence: moderate
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Of 157 participants initially assessed, 137 were enrolled in the Age-Well clinical trial, and 127 were analyzed in this study. 5 key findings →
Design: cross-sectional Participants: 157 Evidence: high
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During 1 110 831 person-years at risk, we recorded 245 573 hospitalisations in the Finnish cohorts; the corresponding numbers in the UK study were 60 946 hospitalisations in 186 572 person-years. 4 key findings →
Design: cohort study Participants: 9,838 Evidence: moderate
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It has been reported that social engagement may be associated with dementia risk. 4 key findings →
Design: case-control study Participants: 31 Evidence: moderate
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The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. 1 key finding →
Design: cohort study Participants: 6,894 Evidence: moderate
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This study found no evidence of a neuroprotective effect of physical activity. 4 key findings →
Design: cohort study Participants: 329 Evidence: moderate
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Low SES substantially increased the risk of dementia and cognitive dysfunction, suggesting that public health strategies could reduce the dementia burden by reducing social inequalities. 4 key findings →
Design: meta-analysis Participants: 1,485,702 Evidence: high
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The overall conversion rate from iRBD to an overt neurodegenerative syndrome was 6.3% per year, with 73.5% converting after 12-year follow-up. 5 key findings →
Participants: 1,280 Evidence: moderate
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The association between metabolic syndrome (MetS) and incident dementia remains inconclusive. 4 key findings →
Design: prospective cohort Participants: 5,255 Evidence: moderate
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Cohort studies have reported that midlife high total serum cholesterol (TC) is associated with increased risk of Alzheimer's disease (AD) in late-life but findings have been based on few studies and previous reviews have been limited by a lack of compatible data. 4 key findings →
Design: meta-analysis Participants: 23,338 Evidence: high
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Midlife and late-life risk factors contributed to 22.7% and 16.5% of total dementia cases, respectively. 5 key findings →
Design: meta-analysis Participants: 37,931 Evidence: high
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Pooled HRs indicated depression present in late-life (HR 1.95, 95% CI: 1.68–2.26; I 2 = 77.5%) and midlife (HR 1.56, 95% CI: 1.12–2.18; I 2 = 97.5%) significantly increased risk of all-cause dementia. 2 key findings →
Design: meta-analysis Participants: 901,762 Evidence: high
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In this study, several factors, mostly modifiable, were associated with a higher risk of YOD. 4 key findings →
Design: cohort Participants: 356,052 Evidence: moderate
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High UPF consumption is associated with dementia. 4 key findings →
Design: meta-analysis Participants: 867,316 Evidence: moderate
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Circulating NfL and GFAP may, independently and jointly, provide useful clinical insight regarding dementia risk and prognosis. 4 key findings →
Design: cohort Participants: 1,712 Evidence: moderate
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Of these, 4361 (8.4%) developed dementia compared with 6610 patients with NTT (5.9%) (P Conclusions and relevance Among patients evaluated in the ED or inpatient settings, those with moderate to severe TBI at 55 years or older or mild TBI at 65 years or older had an increased risk of developing dementia. 3 key findings →
Design: cohort study Participants: 164,661 Evidence: moderate
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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.
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.
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 30,580 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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