27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
After a median of 4.7 years of follow-up, the rate of cardiovascular disease was 10.7 events per 1000 person-years in the aspirin group and 11.3 events per 1000 person-years in the placebo group (hazard ratio, 0.95; 95% confidence interval [CI], 0.83 to 1.08). 4 key findings →
Participants: 19,114 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There was no evidence that aspirin was effective in reducing risk of dementia, MCI, or cognitive decline. 2 key findings →
Participants: 19,114 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Older adults with higher triglyceride levels within the normal to high-normal range had a lower dementia risk and slower cognitive decline over time compared with individuals with lower triglyceride levels. 5 key findings →
Design: randomized controlled trial Participants: 13,976 Evidence: high
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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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Recruitment ended in December 2014 with 16,703 Australian and 2,411 U.S. participants, a median age of 74 (range 65-98) years and 56% women. 1 key finding →
Evidence: high
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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
Full summary, score breakdown and related studies → Original source Free full text
Low-dose aspirin did not prevent depression in this large-scale study of otherwise healthy older adults. 3 key findings →
Participants: 114 Evidence: high
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Whether novel risk variants of Alzheimer's disease (AD) identified through genome-wide association studies also influence magnetic resonance imaging-based intermediate phenotypes of AD in the general population is unclear. 4 key findings →
Design: meta-analysis Participants: 8,175 Evidence: high
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Baseline assessments were conducted on 128 participants. 3 key findings →
Design: randomized controlled trial Participants: 125 Evidence: high
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Identification of individuals with increased risk of major adverse cardiovascular events (MACE) is important. 1 key finding →
Design: randomized controlled trial Participants: 18,548 Evidence: high
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In an older cohort with low cerebrovascular disease burden, T2DM contributes to cognitive decline via neurodegeneration. 3 key findings →
Design: longitudinal study Participants: 124 Evidence: moderate
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T2DM may promote neurodegeneration independent of AD dementia diagnosis, and its effect may be driven by tau phosphorylation. 4 key findings →
Design: cross-sectional Participants: 816 Evidence: low
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Sixteen men and 24 women diagnosed with Alzheimer's disease participated in the study. 3 key findings →
Design: randomized controlled trial Evidence: high
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The MAXCOG intervention is effective in improving goal performance and satisfaction in clients with MCI and early dementia. 2 key findings →
Design: randomized controlled trial Participants: 55 Evidence: high
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Chronic musculoskeletal pain has been linked to dementia; however, chronic pain typically occurs in multiple sites; therefore, this study was to investigate whether greater number of chronic pain sites is associated with a higher risk of dementia and its subtypes. 4 key findings →
Participants: 356,383 Evidence: low
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In this multi-cohort study of older adults without cognitive impairment, we show that WMH and lacunes independently predict increased risk of MCR, after adjusting for key confounders. 5 key findings →
Design: cohort study Participants: 1,772 Evidence: moderate
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Population health research is increasingly focused on the genetic determinants of healthy ageing, but there is no public resource of whole genome sequences and phenotype data from healthy elderly individuals. 4 key findings →
Evidence: moderate
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Lifestyle behavioral change is a critical component for secondary prevention of stroke. 1 key finding →
Design: longitudinal study Evidence: high
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Intronic expansion of a hexanucleotide GGGGCC repeat in the chromosome 9 open reading frame 72 (C9ORF72) gene is the major cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 1 key finding →
Evidence: low
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Here we elucidate the effect of Alzheimer disease (AD)-predisposing genetic backgrounds, APOE4, PSEN1ΔE9, and APPswe, on functionality of human microglia-like cells (iMGLs). 4 key findings →
Evidence: low
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Thirty medical specialists (geriatricians, n = 23; psychiatrists, n = 4; neurologists, n = 3) from 30 different clinics participated (public, 76.7%; private, 23.3%), including from metropolitan (73.3%), regional (20.0%) and rural (6.7%) areas. 5 key findings →
Design: cross-sectional Participants: 23 Evidence: low
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The results indicate that a-MCI and na-MCI display a stable pattern of deficits to attention, working memory, and executive function. 3 key findings →
Design: longitudinal study Evidence: moderate
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Age and female sex are risk factors for dementia, and menopause is associated with cognitive dysfunction. 4 key findings →
Design: cross-sectional Evidence: low
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This review recounts the definitions and research evidence supporting the multifaceted roles of neuroinflammation in the injured brain following trauma. 4 key findings →
Evidence: low
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There were observable geographic variations in education (range 13.4-16.2 years, Figure 1), age (range 66.7-72.4 years) and severable modifiable risk factors for dementia across Tasmania, Australia. 5 key findings →
Design: longitudinal study Participants: 8,891 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. 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 →