Vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of WMLs. 2 key findings →
Participants: 123 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Vascular care in patients with Alzheimer disease with cerebrovascular lesions slows progression of WMLs. 2 key findings →
Participants: 123 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Acceleration in WMH burden, a common indicator of cerebrovascular disease in the elderly, is a pathologic change that emerges early in the presymptomatic phase leading to MCI. 2 key findings →
Design: longitudinal study Participants: 134 Evidence: moderate
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Baseline DBP and longitudinal increases in DBP were independently associated with a greater WMHV, and the association between DBP and WMHV was greatest among blacks. 4 key findings →
Design: longitudinal study Participants: 1,281 Evidence: moderate
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White matter lesions are frequently found on cerebral MRI scans of elderly people and are thought to be important in the pathogenesis of dementia. 5 key findings →
Design: cross-sectional Participants: 1,077 Evidence: low
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Aortic stiffness increases with age and vascular risk factor exposure and is associated with increased risk for structural and functional abnormalities in the brain. 5 key findings →
Participants: 668 Evidence: low
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Higher levels of VRFs were associated with poorer brain health across grey and white matter macrostructure and microstructure. 5 key findings →
Participants: 9,722 Evidence: low
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We postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposits, is associated with cortical tissue loss independent of parenchymal Alzheimer's disease pathology. 4 key findings →
Design: case-control study Participants: 63 Evidence: moderate
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Thirty percent of the cases had significant cerebrovascular parenchymal pathology scores (CVDPS), 54% had significant AD pathology, and 18% had HS. 4 key findings →
Design: longitudinal study Evidence: moderate
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Based on the title and abstracts, 830 papers were screened from which 250 primary research papers met the eligibility criteria (original research articles with patients or with a strict diabetes model without comorbidities, that included direct data about microglia in the brain or retina), and 17 additional research papers were included through forward and backward citations, resulting in a total of 267 primary research articles included in the scoping systematic review. 5 key findings →
Design: systematic review Participants: 267 Evidence: high
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Regular voluntary exercise has been shown to increase waste transport through the glymphatic system in mice. 4 key findings →
Design: cohort Evidence: preliminary
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This should be considered when designing protocols for amyloid-modifying clinical trials. 1 key finding →
Design: longitudinal study Evidence: moderate
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New consensus diagnostic criteria for TES were developed with a primary goal of facilitating future CTE research. 2 key findings →
Participants: 298 Evidence: low
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Aging-associated WMHs evolve significantly over a 4-year period. 5 key findings →
Design: longitudinal study Participants: 150 Evidence: moderate
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Cerebral microbleeds (CMBs) are increasingly recognised neuroimaging findings in individuals with cerebrovascular disease and dementia, and in normal ageing. 1 key finding →
Evidence: low
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Microbleed prevalence was 15.3% (median [interquartile range] count, 1 [1-88]). 5 key findings →
Participants: 4,841 Evidence: low
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Graph theoretical analysis of the speech/language network showed that regions with shorter functional paths to the epicentre exhibited greater longitudinal atrophy. 4 key findings →
Design: longitudinal study Participants: 30 Evidence: moderate
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Cerebral small vessel disease is a major cause of stroke and dementia, but its genetic basis is incompletely understood. 4 key findings →
Participants: 42,310 Evidence: low
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Portable, low‐field imaging could be useful for identifying moderate to severe WMHs. 4 key findings →
Design: prospective cohort Participants: 33 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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Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. 2 key findings →
Evidence: low
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Imaging patterns of atrophy in CBS vary according to pathologic diagnosis. 4 key findings →
Design: case-control study Participants: 24 Evidence: moderate
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In a large community-based sample of middle-aged adults, BI predicted an increased risk of stroke and dementia independent of vascular risk factors. 5 key findings →
Participants: 1,694 Evidence: moderate
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Changes in the properties of DTI may be the potential mechanism of WMH-related MCI, especially the right IFOF and the right ILF, which may become imaging markers for predicting WMH-related cognitive dysfunction. 2 key findings →
Design: longitudinal study Participants: 22 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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Delirium is a profound neuropsychiatric disturbance precipitated by acute illness. 4 key findings →
Design: longitudinal study Participants: 465 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.
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →