White matter findings were significantly associated with age, silent stroke, hypertension, FEV1, and income.
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
White matter findings were significantly associated with age, silent stroke, hypertension, FEV1, and income.
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We determined the frequency of dementia in a cohort of 251 patients aged greater than or equal to 60 years hospitalized with acute ischemic stroke, based on examinations performed 3 months after stroke onset. 5 key findings →
Participants: 251 Evidence: moderate
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Arterial spin labeling (ASL) is a non-invasive MRI technique to measure cerebral blood flow (CBF). 5 key findings →
Design: longitudinal study Evidence: moderate
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Uncontrolled diabetes increases the risk of Alzheimer's disease and VaD. 4 key findings →
Participants: 1,248 Evidence: moderate
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Older adults with dementia who take atypical antipsychotics have a similar risk of ischaemic stroke to those taking typical antipsychotics. 1 key finding →
Design: cohort study Evidence: moderate
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However, whether large perivascular spaces (L-PVSs) (>3 mm in diameter) visible on MRI are associated with SVD and cognitive deterioration in older individuals is unknown. 5 key findings →
Participants: 2,612 Evidence: low
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The small effect of VRFs and LAD on WMH suggests that WMH have a large "nonvascular," nonatheromatous etiology. 3 key findings →
Participants: 881 Evidence: moderate
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There are specific risk factors associated with feeding tube placement in nursing home residents with severe cognitive impairment. 4 key findings →
Design: cohort study Evidence: moderate
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Although concerns about increased bleeding risk with combined warfarin-antiplatelet therapy are not unfounded, the risk of bleeding is moderately increased. 2 key findings →
Design: retrospective cohort Evidence: moderate
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Our data suggest that cardiovascular risk factors may modulate the clinical expression of CADASIL. 5 key findings →
Design: prospective cohort Evidence: moderate
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Cerebrovascular reactivity (CVR) deficits may contribute to small vessel disease, such as white matter hyperintensities (WMH). 2 key findings →
Participants: 125 Evidence: low
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G) Functions, such as vessel stabilization, regulation of vascular tone and maintenance of local and tissue homeostasis (contractile capacity and vessel permeability regulation), matrix protein synthesis, macrophage-like properties, immunological defense, intervention in coagulation, participation in mechanisms that regulate the quiescent and angiogenic stages of blood vessels (including the behaviour of pericytes during sprouting angiogenesis and intussuceptive vascular growth, as well as pericyte interactions with endothelium and other cells, and with extracellular matrix) and plasticity, as progenitor cells with great mesenchymal potential, originating other pericytes, fibroblast/myofibroblasts, preadipocytes, chondroblasts, osteoblasts, odontoblasts, vascular smooth muscle and myointimal cells. 5 key findings →
Design: longitudinal study Evidence: moderate
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SES and LA were associated with better cognitive performance at baseline, but were not associated with cognitive decline over time. 5 key findings →
Design: longitudinal study Participants: 181 Evidence: moderate
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In the Research Article "Magnitude and Time-Course of Dementia Risk in Stroke Survivors: A Population-Wide Matched Cohort Study" by Joundi et al., 1 the keys for Figure 3, A-D should indicate red for "Stroke," "Ischemic Stroke," "ICH," and "Stroke," respectively. 2 key findings →
Design: cohort study Evidence: moderate
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The text describes cerebral small vessel disease as a group of pathological processes affecting the brain's small vessels, with age-related and hypertension-related forms and cerebral amyloid angiopathy being most common. 3 key findings →
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The etiology of cerebrovascular pathology is heterogeneous. 3 key findings →
Participants: 29 Evidence: low
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No significant differences of VRFs were identified between DLB and AD. 5 key findings →
Participants: 363 Evidence: low
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The final model, which included age, systolic blood pressure >140, atrial fibrillation, and tobacco use, achieved an AUC of 0.83 (95% CI 0.75-0.90) in the development cohort (N=143, 62.4±12.6 years, 44% female, 36% non-white race) and 0.85 (95% CI 0.77-0.92) in the validation cohort (N=127, 65.2±16.8 years, 51% female, 34% non-white race), with similar results using WMH measurements derived from cMRI (N=120, p=0.98, AUC=0.86, 95% CI 0.77-0.93). 5 key findings →
Participants: 143 Evidence: moderate
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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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In SPRINT, the overall interaction between age and SBP on WMHv change was not statistically significant ( P =0.18). 5 key findings →
Design: longitudinal study Participants: 172 Evidence: moderate
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A total of 261 patients (75.3±6.8 years) were recruited from a memory-clinic cohort. 5 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau. 5 key findings →
Design: longitudinal study Participants: 494 Evidence: moderate
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Twenty-four patients of comparable age, blood pressure, and degree of dementia were classified by an "Ischemic Score" based on clinical features into "multi-infarct" and "primary degenerative" dementia. 5 key findings →
Evidence: low
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Accumulating evidence implicates small vessel cerebrovascular disease, visualized as white matter hyperintensities (WMH) on T2-weighted magnetic resonance imaging, in the pathogenesis and diagnosis of Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional Participants: 26 Evidence: moderate
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In the absence of other prior neurologic insult, both AD and other dementias increase the risk of generalized- and partial-onset unprovoked seizures. 2 key findings →
Design: case-control study 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 →