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Find studies

Showing 51–73 of 73 studies in Vascular contributions of type cohort or longitudinal study (page 3 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 73 studies, in this order: BibTeX (.bib) · RIS (.ris)

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.

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

Effect of Intensive Systolic Blood Pressure Control on Markers of Cerebral Small Vessel Disease by Age

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Hypertension 2025-10-29

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

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

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

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

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

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

Design: longitudinal study Evidence: moderate

Impact of regional white matter hyperintensity patterns on cognitive trajectories in NACC

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Alzheimer s & Dementia 2025-10-01

Five WMH clusters emerged. Compared to those with low WMH burden, participants in the mild occipital and high parieto-occipital clusters had faster memory decline; mild fronto-parietal and high parieto-occipital clusters showed faster executive decline; and mild and high fronto-parietal and high parieto-occipital clusters had faster language decline. 5 key findings →

Design: longitudinal study Participants: 1,047 Evidence: moderate

= 0.025) over 3 years. NfL was not significantly associated with any MRI cSVD marker. 5 key findings →

Design: longitudinal study Evidence: moderate

This validated nomogram incorporating clinical, biochemical, and neuroimaging biomarkers provides a robust tool for individualized PSCIND risk assessment in first-ever MIS patients, with potential to guide targeted interventions and cognitive monitoring. 2 key findings →

Design: cohort study Participants: 137 Evidence: moderate

BackgroundThe progression of cerebral small vessel disease (CSVD) leads to cognitive decline, which can be categorized into subcortical vascular mild cognitive impairment (svMCI) and vascular dementia (VaD).ObjectiveThis research aimed to examine the structural changes in gray (GM) and white matter (WM) in the brain across the disease spectrum. 5 key findings →

Design: longitudinal study Participants: 26 Evidence: moderate

The glymphatic system, a vital brain perivascular network for waste clearance, hinges on the functionality of the aquaporin 4 (AQP4) water channel. 5 key findings →

Design: longitudinal study Evidence: moderate

=0.002). Early-onset CHD and genetic susceptibility are associated with a higher risk of incident dementia and a larger WMH volume. 2 key findings →

Design: cohort study Participants: 671 Evidence: moderate

Pulse pressure, but not mean arterial pressure, significantly mediated the relationship between age and white matter hyperintensity load. 5 key findings →

Design: cohort study Evidence: moderate

Individuals with msWMH showed systematic deficits in face-memory processing across encoding, maintenance, and retrieval, accompanied by reduced theta power and synchronization, altered alpha power, and disrupted theta-gamma coupling. 5 key findings →

Design: longitudinal study Evidence: moderate

Older stroke survivors engaging in regular PA had a 38 % reduced risk of dementia [Odds Ratio (OR) =0.62, 95 % Confidence Interval (CI): 0.56-0.69, P < 0.001] and a 44 % lower risk of mortality [Hazard Ratio (HR) =0.56, 95 % CI: 0.52-0.59, P < 0.001]. 5 key findings →

Design: longitudinal study Evidence: moderate

Incidental covert cerebral small vessel disease: Detection and management

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Advanced Neurology 2025-01-16

Cerebral small vessel disease (CSVD) is one of the most common vascular diseases of the brain, primarily diagnosed using magnetic resonance imaging biomarkers. 5 key findings →

Design: longitudinal study Evidence: moderate

Depth-Dependent Alterations in Cerebral Blood and Tissue Oxygenation Associated with Tau in Alzheimer’s Disease Models

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-16

Vascular dysfunction is increasingly recognized as a feature of Alzheimer’s disease (AD), and inadequate oxygen delivery may contribute to neuronal death. 5 key findings →

Design: longitudinal study Evidence: moderate

Generalizing Amyloid β Pathology from Postmortem Human Brains with Vision Foundation Models for Lesion Quantification

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-07

The ViTamyloid classifier achieved strong feature-separation metrics, yielding area under the receiver operating characteristic curve (AUROC) and precision-recall curve (AUPRC) values of 0.994/0.958 for CCP, 0.989/0.945 for CGP, 0.992/0.977 for CAA Type 1, and 0.997/0.978 for CAA Type 2. 4 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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