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Find studies

Showing 126–150 of 546 studies in Vascular contributions (page 6 of 22) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

What “Vascular contributions” covers

Vascular contributions — How blood vessel health, small-vessel disease and stroke risk contribute to dementia and cognitive decline.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Heavy smoking in midlife and long-term risk of Alzheimer disease and vascular dementia

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of internal medicine 2010-10-25

In this large cohort, heavy smoking in midlife was associated with a greater than 100% increase in risk of dementia, AD, and VaD more than 2 decades later. 5 key findings →

Participants: 5,367 Evidence: moderate

Among 2935 patients (50.4% women; mean age=72.2 years; 19.8% subjective cognitive impairment, 39.8% mild cognitive impairment, and 40.4% dementia), larger WMH volume within projection fibres (B=0.24, SE=0.10, p=0.013) was associated with greater apathy. 5 key findings →

Participants: 2,935 Evidence: low

Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. 2 key findings →

Participants: 40,000 Evidence: low

Our aim is to examine the interplay between cerebral small vessel disease (CSVD) pathology, Alzheimer’s disease (AD) related amyloid-β (Aβ) clearance, and cognition in general population. 2 key findings →

Design: cross-sectional Participants: 1,026 Evidence: moderate

This study included 3540 participants with RVC data and 489 with WMH data (median [IQR] age: 73.2 [71.4-76.3] and 72.5 [71.2-75.4] years; female: 52.9% and 47.6%) over a median follow-up of 7.4 [IQR 5.5-8.5] and 3.8 [IQR 2.9-5.3] years, respectively. 5 key findings →

Design: cross-sectional Participants: 3,540 Evidence: moderate

Out of 462,327 eligible participants, those with constipation were associated with higher incidence of three outcome diseases (1415/20,263 [7.0%]) than those without (18,848/442,064 [4.3%]), with adjusted hazard ratio (HR) being 1.35 [1.27-1.42]. 5 key findings →

Design: cohort study Evidence: moderate

Examining multimorbidity contributors to dementia over time

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Alzheimer s & Dementia 2025-02-01

Hypertension, acute myocardial infarction, atrial fibrillation, diabetes, heart failure, ischemic heart disease, stroke, and arthritis additively accounted for 71.8% (95% confidence interval [CI]: 62.9%-79.1%) of ADRD incident cases based on LE-AAF. 5 key findings →

Design: longitudinal study Evidence: moderate

Dementia after ischemic stroke: a population-based study in Rochester, Minnesota (1960-1984)

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 1996-01-01

We used the medical records linkage system for the population of Rochester, Minnesota, to identify persons in the community who had their first cerebral infarct without previous dementia. 2 key findings →

Participants: 971 Evidence: moderate

Some patients receiving oral anticoagulation therapy are more challenging to maintain within the therapeutic range than others. 2 key findings →

Participants: 124,619 Evidence: low

Our results suggest that genes associated with clinical neurological disease also have detectable effects on subclinical phenotypes. 5 key findings →

Participants: 705 Evidence: low

We found that 451 (92.8%) of the patients were testable, 239 (49.2%) of the patients were women, and the mean age was 71.2 years. 5 key findings →

Participants: 486 Evidence: moderate

The aging population is increasing and, therefore, a higher prevalence of cardiac disease is emerging; including hypertension, coronary artery disease, atrial fibrillation and chronic heart failure. 1 key finding →

Design: cohort study Evidence: moderate

Relationship between white matter hyperintensities, cortical thickness, and cognition

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Stroke 2015-01-08

These cross-sectional results suggest that cortical changes (regional-specific damage and network breakdown), mediated (in)directly by WMH (tract-specific damage) and other factors (eg, vascular risk factors), might lead to cognitive decline. 5 key findings →

Design: cross-sectional Participants: 426 Evidence: low

A total of 124 participants with Alzheimer disease, cerebrovascular disease, or a mix Alzheimer's and cerebrovascular diseases and 55 controlparticipants underwent magnetic resonance imaging and neuropsychological testing. 5 key findings →

Participants: 124 Evidence: low

Alzheimer's disease (AD) is characterized by senile plaques and neurodegeneration although the neurotoxic mechanisms have not been completely elucidated. 3 key findings →

Design: longitudinal study Evidence: moderate

White matter hyperintensity (WMH), indicative of cerebral small vessel disease, has emerged as a potential biomarker for cognitive decline in Alzheimer's disease (AD). 2 key findings →

Design: cross-sectional Participants: 158 Evidence: low

Considerable data support the presence of both systemic and CNS inflammation in SVD and VCID. 3 key findings →

Design: longitudinal study Evidence: moderate

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Where “Free full text” comes from

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

How the 0–100 score works — and why some entries are capped

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.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

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.

What this library is — and isn't

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 →

Newest studies, as a dated timeline →    Atom feed