27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We tested the hypothesis that a causal relationship exists between systolic BP (SBP) and/or diastolic BP (DBP) and risk of Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Participants: 299,024 Evidence: high
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Socioeconomic factors and genetic predisposition are established risk factors for dementia. 4 key findings →
Design: cohort study Participants: 196,368 Evidence: moderate
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Men have a shorter life expectancy compared with women but the underlying factor(s) are not clear. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
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There was a significant interaction (P = 0.024) between B vitamin treatment and plasma combined ω-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) on brain atrophy rates. 5 key findings →
Participants: 83 Evidence: low
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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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A total of 2320 unique papers was found; the full text of 87 was reviewed. 1 key finding →
Design: systematic review Participants: 10,500 Evidence: high
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Of 6 952 440 vaccinated patients in the derivation cohort, 5 150 310 (74.1%) had two vaccine doses. 4 key findings →
Design: cohort study Evidence: moderate
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Individual conditions have been identified as risk factors for dementia; however, it is important to consider the role of multimorbidity, as conditions often co-occur. 4 key findings →
Design: cohort study Participants: 960 Evidence: moderate
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Review of the evidence and recommendations are provided for the diagnosis of osteoporosis, fracture-risk assessment and intervention thresholds, management of vertebral fractures, non-pharmacological and pharmacological treatments, including duration and monitoring of anti-resorptive therapy, glucocorticoid-induced osteoporosis, as well as models of care for fracture prevention. 5 key findings →
Design: meta-analysis Evidence: high
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Our findings showed significant associations between hearing and vision impairments and increased risks of all-cause and cause-specific dementia. 5 key findings →
Design: meta-analysis Participants: 937,908 Evidence: moderate
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Prospective, population-based studies that recruit participants in mid-life are valuable resources for dementia research. 1 key finding →
Participants: 500,000 Evidence: low
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Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →
Evidence: low
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The impact of Parkinson's disease (PD) dementia is substantial and has major functional and socioeconomic consequences. 4 key findings →
Design: longitudinal study Participants: 486 Evidence: moderate
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Data were drawn from the UK Biobank cohort study with a total of 228 223 participants with Hospital Episodes Statistics and primary care linkage health records. 4 key findings →
Design: cohort study Participants: 2,378 Evidence: moderate
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Researchers conducted a large, two-stage meta-analysis of genome-wide association studies in individuals of European ancestry.
Evidence: low
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This study undertook a two-stage genome-wide association study (GWAS) of Alzheimer's disease involving over 16,000 individuals. 4 key findings →
Evidence: low
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The authors sought to identify new susceptibility loci for Alzheimer's disease through a staged association study and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium in a companion paper. 2 key findings →
Evidence: low
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PRT may have a small beneficial effect on cognitive function in SVCI. 5 key findings →
Design: RCT Participants: 91 Evidence: early
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Overall, 318 patients with AD completed BPST with an improvement of 5.6 points on the total Cohen-Mansfield Agitation Inventory (CMAI; mean [SD], 63.3 [16.0] to 57.7 [18.4], t = 4.8, df = 317, p 95% of patients. 2 key findings →
Design: randomized controlled trial Participants: 318 Evidence: high
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Serum tHcy levels were significantly higher and serum folate and vitamin B12 levels were lower in patients with DAT and patients with histologically confirmed AD than in controls. 4 key findings →
Design: case-control study Participants: 164 Evidence: moderate
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The category of neocortical LP according to the LPC system was associated with a 5.9 OR (p < 0.0001) of dementia in the 134 NBTR cases and a 3.14 OR (p = 0.0001) in the 202 UPBB cases. 2 key findings →
Participants: 202 Evidence: low
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Incidence of dementia is nearly 50 times higher in the year after a major stroke compared with that in the general population, but excess risk is substantially lower after transient ischaemic attack and minor stroke. 1 key finding →
Participants: 728 Evidence: low
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The preponderance of epidemiologic and tissue compositional studies supports a protective effect of omega-3 EFA intake, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in mood disorders. 3 key findings →
Design: meta-analysis Evidence: high
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Previous studies have suggested that systemic viral infections may increase risks of dementia. 4 key findings →
Design: case-control study Evidence: moderate
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →