CNS small vessel disease (CSVD) causes 25% of strokes and contributes to 45% of dementia cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
CNS small vessel disease (CSVD) causes 25% of strokes and contributes to 45% of dementia cases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings in CPAP+ participants suggest that CPAP treatment of SDB may delay progression of cognitive impairment. 4 key findings →
Evidence: moderate
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These cases illustrate that the alpha-synuclein pathogenic process may start decades before the first symptoms of PD, DLB, or MSA. 1 key finding →
Participants: 27 Evidence: low
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In a clinical sample, patients with nonamnestic MCI were more likely to develop DLB, and those with amnestic MCI were more likely to develop probable AD. 1 key finding →
Participants: 337 Evidence: moderate
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Blood pressure variability is an emerging risk factor for cognitive decline and dementia, but mechanisms remain unclear. 4 key findings →
Design: cohort study Evidence: moderate
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A total of 533 patients with AD at early stages (mean Folstein Mini-Mental State Examination [MMSE] 21/30 at entry) were recruited and followed semiannually for up to 13.1 years (mean 3) in five University-based AD centers in the United States and European Union. 4 key findings →
Participants: 533 Evidence: moderate
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The sample included dementia-free participants (mean age 40 ± 9 years; 53% women) of the Framingham Heart Study third-generation cohort with cognitive testing of memory, abstract reasoning, visual perception, attention, and executive function (n = 2,126). 4 key findings →
Participants: 2,126 Evidence: moderate
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(n = 2,392) had a mean age of 74.4 years, 60.4% were female, and 17.1% were of self-reported Black race. 5 key findings →
Design: cross-sectional Participants: 2,392 Evidence: low
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There were 13,145 individuals with risk factor data between 2015 and 2018 (51.1% aged 18-44, 31.0% aged 45-64, and 17.9% aged ≥65 years; 51.5% female after survey-weighting). 5 key findings →
Design: cross-sectional Participants: 13,145 Evidence: low
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The study included 356,173 participants (median age 56 years; 53.69% female). 5 key findings →
Participants: 356,173 Evidence: low
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< 0.01). Using an operationalization of clinical criteria for LATE, 8.2% of participants with MCI or dementia from our tertiary memory clinic were classified as Possible-LATE, Probable-LATE, or LATE-AD. 4 key findings →
Design: longitudinal study Evidence: moderate
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The analytic sample included 469 participants (mean age 71.2 ± 8.5 years, 53% female). 3 key findings →
Design: cohort Participants: 469 Evidence: early
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We describe a 2-feature biomarker approach to classifying elderly CN subjects that is complementary to the National Institute on Aging-Alzheimer's Association preclinical staging criteria. 2 key findings →
Participants: 252 Evidence: low
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Individuals with early AD show heterogeneity in disease progression, which increases when stratifying on risk factors associated with progression. 3 key findings →
Participants: 302 Evidence: low
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Our results reveal a spatial association between the epileptogenic focus and tau deposition, amyloid deposition, and neurodegeneration in early clinical stages of AD. 5 key findings →
Design: cross-sectional Evidence: low
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Midlife NAFLD shows associations with AD and accumulating vascular pathology, revealing potential pathways linking liver function to dementia. 2 key findings →
Participants: 1,706 Evidence: low
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The combined measure of CSF Abeta42 and tau meets the requirements for clinical use in discriminating AD from normal aging and specific neurologic disorders. 4 key findings →
Participants: 84 Evidence: low
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PIB-positive subjects with mild cognitive impairment (MCI) are significantly more likely to convert to AD than PIB-negative patients, faster converters having higher PIB retention levels at baseline than slower converters. 4 key findings →
Evidence: low
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The proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71% (60/85) in A-N-, A+N-, SNAP, and A+N+, respectively; the proportion of APOE ε4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A+N- and A+N+ groups (p ≤ 0.005). 2 key findings →
Participants: 201 Evidence: low
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Logopenic progressive aphasia (LPA) is a distinctive variant of primary progressive aphasia. 4 key findings →
Evidence: low
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Differences in white matter hyperintensities (WMH) associated with increasing cognitive impairment appear related to both extent and spatial location. 5 key findings →
Design: post-hoc analysis Participants: 26 Evidence: low
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Systemic inflammation is associated with ischemia and Alzheimer disease (AD). 3 key findings →
Design: cross-sectional Evidence: low
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Frontotemporal dementia and Alzheimer disease display different spatial distributions of hypoperfusion on arterial spin labeling MRI. 2 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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This cluster analysis of cortical thickness of the entire brain showed that AD dementia in the earlier stages can be categorized into various anatomical subtypes, with distinct clinical features. 5 key findings →
Participants: 52 Evidence: low
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DCTclock discriminates between diagnostic groups and improves upon traditional cognitive tests for detecting biomarkers of amyloid and tau pathology in CN older adults. 3 key findings →
Participants: 300 Evidence: low
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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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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