27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We developed, replicated, and validated an MRI measure of cerebrovascular and neurodegenerative pathologies that are associated with clinical and neuropathologic diagnosis of AD and related to established biomarkers. 5 key findings →
Design: cross-sectional Participants: 1,175 Evidence: moderate
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Insomnia in cognitively unimpaired adults at increased risk for AD is associated to poorer performance in some executive functions and volume changes in cortical and subcortical gray matter, including key areas involved in Alzheimer's disease, as well as decreased white matter diffusivity. 4 key findings →
Design: cross-sectional Participants: 366 Evidence: low
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Of 4413 individuals (mean [SD] age, 71.27 [4.66] years, 2617 women [59.3%]), mean Aβ-PET was elevated in individuals with history of memory impairment in both parents (n = 455; mean [SD] standardized uptake value ratio [SUVR] = 1.12 [0.19]; Wilcoxon P = 1.1 × 10-5) and in those with only maternal history (n = 1772; mean [SD] SUVR = 1.10 [0.19]; Wilcoxon P = 2.70 × 10-5) compared with those with only paternal history (n = 632; mean [SD] SUVR = 1.08 [0.18]; Wilcoxon P = 1.1 × 10-5) or no family history (n = 1554; mean [SD] SUVR = 1.08 [0.19]; Wilcoxon P = 1.1 × 10-5). 3 key findings →
Design: cross-sectional Participants: 455 Evidence: high
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Inclusion and exclusion criteria were met in 303 patients, and 25 (8.3%) presented to the ED with delirium. 1 key finding →
Design: cross-sectional Participants: 303 Evidence: low
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In our training set, people with Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies had lower CSF α-synuclein concentrations than patients with Alzheimer's disease and other neurological disorders. 1 key finding →
Design: cross-sectional Evidence: moderate
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Preclinical AD is associated with rest-activity rhythm fragmentation, independent of age or sex. 5 key findings →
Design: cross-sectional Participants: 205 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
In this study, females exhibited higher tau compared with age-matched males, particularly in the setting of elevated Aβ. 5 key findings →
Design: cross-sectional Evidence: low
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The prevalence of dementia, AD, and VaD among individuals aged 65 years and older were 5.14% (95% CI, 4.71-5.57), 3.21% (95% CI, 2.87-3.55), and 1.50% (95% CI, 1.26-1.74), respectively. 2 key findings →
Design: cross-sectional Participants: 6,096 Evidence: low
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In this diverse community-based cohort, cross-sectional data revealed significant race/ethnic disparities in the prevalence of MCI and dementia. 3 key findings →
Design: cross-sectional Participants: 989 Evidence: moderate
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The relation of blood pressure with cognitive function and dementia has, in recent years, received much attention from epidemiological research. 2 key findings →
Design: cross-sectional Evidence: high
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Hearing loss is independently associated with lower scores on tests of memory and executive function. 5 key findings →
Design: cross-sectional Participants: 347 Evidence: moderate
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The structure and integrity of the ageing brain is interchangeably linked to physical health, and cardiometabolic risk factors (CMRs) are associated with dementia and other brain disorders. 4 key findings →
Design: cross-sectional Evidence: high
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Silent brain infarcts and white matter lesions are frequently seen on magnetic resonance imaging in healthy elderly people and both are associated with an increased risk of stroke and dementia. 5 key findings →
Design: cross-sectional Participants: 1,077 Evidence: low
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Older Medicare beneficiaries in California with DS, especially those with dementia, have a high level of multimorbidity including several treatable conditions. 3 key findings →
Design: cross-sectional Participants: 100 Evidence: low
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Synaptic loss is an early pathologic substrate of Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 38 Evidence: moderate
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Core CSF changes in Alzheimer disease (AD) are decreased amyloid β(1-42), increased total tau, and increased phospho-tau, probably indicating amyloid plaque accumulation, axonal degeneration, and tangle pathology, respectively. 4 key findings →
Design: cross-sectional Participants: 529 Evidence: moderate
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Cognitive assessments after stroke are typically short form tests developed for dementia that generates pass/fail classifications (e.g. the MoCA). 4 key findings →
Design: cross-sectional Evidence: low
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A total of 621 participants (aged 69.9 ± 3.8, 71% female) had available data for the main analyses and 355 had PET Centiloid data available. 5 key findings →
Design: cross-sectional Participants: 621 Evidence: high
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Longitudinal analysis identified significant associations between the change in ether lipid species (including alkylphosphatidylcholine, alkenylphosphatidylcholine, lysoalkylphosphatidylcholine, and lysoalkenylphosphatidylcholine) and AD dementia conversion. 5 key findings →
Design: cross-sectional Participants: 1,393 Evidence: moderate
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Brain regions with higher synaptic density are associated with a higher 18F-AV-1451 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminishes with disease severity. 1 key finding →
Design: cross-sectional Participants: 12 Evidence: moderate
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These findings provide support for both the feasibility and validity of C3 and computerized cognitive outcomes more generally in AD secondary prevention trials. 3 key findings →
Design: cross-sectional Participants: 4,486 Evidence: low
Full summary, score breakdown and related studies → Original source
For amyloid positron emission tomography positive (Aβ+) subjects, flortaucipir neocortical standard uptake value ratio was significantly higher with more advanced clinical stage (Alzheimer's disease > mild cognitive impairment > older cognitively normal) and was significantly elevated for Aβ+ mild cognitive impairment and Alzheimer's disease subjects relative to the respective Aβ- subjects. 5 key findings →
Design: cross-sectional Participants: 217 Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated plasma neurofilament light chain (NfL) is associated with dementia though underlying mechanisms remain unknown. 3 key findings →
Design: cross-sectional Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundDiabetes has been linked to increased prevalence of dementia, but the link between diabetic retinopathy (DR) and Alzheimer's disease (AD) remains unclear. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source
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 →