28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 2846 articles identified, 94 studies were eligible, with up to 14 529 participants for WMH, 16 012 participants for BI, 15 693 participants for CMB, and 4587 participants for PVS. 2 key findings →
Design: meta-analysis Participants: 529 Evidence: high
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This large GWAS of WMH burden in community-based cohorts of individuals of European descent identifies a novel locus on chromosome 17. 5 key findings →
Design: meta-analysis Participants: 3,024 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Periventricular white matter hyperintensities (WMH; PVWMH) and deep WMH (DWMH) are regional classifications of WMH and reflect proposed differences in cause. 4 key findings →
Design: meta-analysis Participants: 26,654 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
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We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms. 2 key findings →
Design: meta-analysis Participants: 17 Evidence: high
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MoCA was administered to 274 patients from 2 prospective hospital-based cohort studies in Germany (n = 125) and France (n = 149). 4 key findings →
Design: cohort study Participants: 125 Evidence: moderate
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A total of 16 084 European adults from 8 cohort studies (mean age range, 56.9±12.3-82.1±4.2 years) of the European Eye Epidemiology (E3) consortium. 4 key findings →
Design: meta-analysis Participants: 16 Evidence: high
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An international working group from the Centres of Excellence in Neurodegeneration completed a structured process to develop definitions and imaging standards for markers and consequences of cerebral small vessel disease (SVD). 3 key findings →
Evidence: low
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WMHs in the frontoparietal and anterior periventricular region were associated with blood pressure traits, WMH genetic risk score (GRS), baseline and decline in general cognitive performance, incident all-cause dementia, and ischemic stroke. 5 key findings →
Design: longitudinal study Participants: 2,878 Evidence: moderate
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Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →
Participants: 49 Evidence: low
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MI failed to show an effect on metabolism in FDG-based AD biomarker, but exploratory analysis suggested positive effect on limbic system metabolism. 4 key findings →
Participants: 67 Evidence: high
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In this large cohort study of elderly subjects, the degree of dVRS appears independently associated with age, hypertension, volume of white matter hyperintensities, and lacunar infarctions. dVRS should be considered as another MRI marker of cerebral small vessel disease in the elderly with regional variations in their severity. 4 key findings →
Design: cohort study Evidence: moderate
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Brain macrophage populations include parenchymal microglia, border-associated macrophages, and recruited monocyte-derived cells; together, they control brain development and homeostasis but are also implicated in aging pathogenesis and neurodegeneration. 4 key findings →
Evidence: low
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited arterial disease of the brain recently mapped to chromosome 19. 5 key findings →
Participants: 148 Evidence: low
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) has been recently reported as a cause of stroke. 5 key findings →
Evidence: low
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). Moreover, 12 proteins related to endothelial function and inflammation were associated with neuroimaging features of SVD. 4 key findings →
Design: cross-sectional Participants: 35 Evidence: moderate
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Cortical superficial siderosis describes a distinct pattern of blood-breakdown product deposition limited to cortical sulci over the convexities of the cerebral hemispheres, sparing the brainstem, cerebellum and spinal cord. 4 key findings →
Evidence: low
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Cerebral small vessel disease (SVD) is recognized as a major vascular contributor to cognitive decline, ultimately leading to dementia and stroke. 1 key finding →
Design: longitudinal study Evidence: moderate
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'Covert' cerebral small vessel disease (ccSVD) is common on neuroimaging in persons without overt neurological manifestations, and increases the risk of future stroke, cognitive impairment, dependency, and death. 3 key findings →
Evidence: high
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Cerebrovascular disease typically manifests with stroke, cognitive impairment, or both. 2 key findings →
Evidence: low
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Perivascular spaces include a variety of passageways around arterioles, capillaries and venules in the brain, along which a range of substances can move. 5 key findings →
Evidence: low
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The risk of vascular or mixed dementia, but not of other types of dementia, was significantly increased in MCI patients with a large amount of subcortical hyperintensities at baseline. 5 key findings →
Participants: 170 Evidence: low
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Cohort 1 included 446 individuals (mean age (SD) 65.2 years (8.9); 203 women), Cohort 2 included 164 individuals (mean age (SD) 49.9 years (12.6); 88 women). 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
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Epidemiologic data suggest that individuals at all stages of CKD have a higher risk of developing cognitive disorders and dementia. 1 key finding →
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. 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →