27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Modifiable vascular and lifestyle-related risk factors have been associated with dementia risk in observational studies. 4 key findings →
Design: randomized controlled trial Participants: 631 Evidence: high
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In analyses that addressed bias due to reverse causation, physical inactivity was not associated with all-cause dementia or Alzheimer's disease, although an indication of excess dementia risk was observed in a subgroup of physically inactive individuals who developed cardiometabolic disease. 2 key findings →
Design: meta-analysis Participants: 404 Evidence: high
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In this meta-analysis of the association of physical activity with cognitive decline, physical activity was associated with better late-life cognition, but the association was weak. 5 key findings →
Design: meta-analysis Participants: 341,471 Evidence: moderate
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Median follow-up by intention to treat was 2.0 years. 2 key findings →
Participants: 1,180 Evidence: low
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The APOE ε4 carriers and noncarriers were not significantly different at baseline (except for serum cholesterol level). 5 key findings →
Participants: 1,260 Evidence: high
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PA was associated with lower incidence of all-cause dementia and Alzheimer's disease, even in longer follow-ups, supporting PA as a modifiable protective lifestyle factor, even after reducing the effects of reverse causation. 5 key findings →
Design: meta-analysis Participants: 257,983 Evidence: moderate
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The FINGER intervention was beneficial regardless of participants' characteristics and can thus be implemented in a large elderly population at increased risk for dementia. 3 key findings →
Participants: 1,260 Evidence: high
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The FINGER is at the forefront of international collaborative efforts to solve the clinical and public health problems of early identification of individuals at increased risk of late-life cognitive impairment, and of developing intervention strategies to prevent or delay the onset of cognitive impairment and dementia. 3 key findings →
Participants: 1,200 Evidence: high
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
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An intensive and long-term exercise program had beneficial effects on the physical functioning of patients with AD without increasing the total costs of health and social services or causing any significant adverse effects. 3 key findings →
Design: randomized controlled trial Participants: 210 Evidence: high
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Vascular dementia is the second commonest form of dementia, and vascular factors contribute to the development of dementia in many patients with Alzheimer's disease. 5 key findings →
Participants: 396 Evidence: low
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Cholinergic deficits might contribute to vascular cognitive impairment. 4 key findings →
Participants: 86 Evidence: high
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Existing studies have included a narrow range of infectious diseases, relied on short follow-up periods, and provided little evidence for whether the increased risk is limited to specific dementia subtypes or attributable to specific microbes rather than infection burden. 5 key findings →
Design: cohort study Participants: 490 Evidence: moderate
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Over a median follow-up of 10·0 years (IQR 5·1-21·3), high physical activity levels were associated with reduced risks of all-cause dementia (n=146 effect sizes; RR 0·80 [95% CI 0·75-0·86]; I 2 =97·4%), Alzheimer's disease (n=59; 0·79 [0·70-0·90]; I 2 =91·3%), and vascular dementia (n=21; 0·71 [0·58-0·87]; I 2 =77·5%); however, associations varied by domain. 3 key findings →
Design: meta-analysis Participants: 4,227,297 Evidence: high
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Among 12,327 patients who underwent randomization (6162 to the asundexian group and 6165 to the placebo group), the incidence of ischemic stroke was lower in the asundexian group than in the placebo group (6.2% vs. 8.4%; cause-specific hazard ratio, 0.74; 95% confidence interval [CI], 0.65 to 0.84; P<0.001). 5 key findings →
Design: clinical trial Participants: 12,327 Evidence: low
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Frailty, comorbidities, and other age-related diseases were associated with a higher risk of dementia but did not account for the elevated dementia risk observed after severe infections. 3 key findings →
Design: cohort Participants: 449,223 Evidence: moderate
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Regular, long-term, customized HE improved the executive function of community-dwelling older people with memory disorders, but the effects were mild and were not observed in other domains of cognition. 3 key findings →
Participants: 210 Evidence: high
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In patients with sporadic ALS, we identified the repeat expansion in 236 (7·0%) of 3377 white individuals from the USA, Europe, and Australia, two (4·1%) of 49 black individuals from the USA, and six (8·3%) of 72 Hispanic individuals from the USA. 1 key finding →
Participants: 4,448 Evidence: low
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Previous studies have shown that limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) increases with age, but there have been only a few studies, which have investigated this entity in a population-based setting. 5 key findings →
Design: cohort Participants: 295 Evidence: moderate
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The treatment of ischaemic stroke with neuroprotective drugs has been unsuccessful, and whether these compounds can be used to reduce disability after recurrent stroke is unknown. 4 key findings →
Participants: 20,332 Evidence: high
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Recent studies suggest that delirium is associated with risk of dementia and also acceleration of decline in existing dementia. 5 key findings →
Participants: 232 Evidence: low
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The genetic basis of Lewy body dementia (LBD) is not well understood. 4 key findings →
Evidence: low
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The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases. 2 key findings →
Evidence: low
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The First Key Symposium was held in Stockholm, Sweden, 2-5 September 2003. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
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 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.
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 →