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43/100

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Vascular contributions

Topic: Inflammation, microglia and astrocytes

Plain-language summary

Cerebral small vessel disease (SVD) is a vascular disorder that increases the risk of stroke and dementia and is diagnosed through brain MRI. Current primary prevention and secondary treatment of SVD are focused on lifestyle interventions and vascular risk factor control, including blood pressure reduction. However, these interventions have limited effects, a proportion of individuals with sporadic SVD do not have hypertension, and SVD shows strong familial and genetic underpinnings. Here, we describe the increasing evidence that cerebral endothelial cell dysfunction is a key mechanism of SVD. Dysfunctional endothelial cells can cause cerebral blood vessel dysfunction, alter blood-brain barrier integrity and interfere with cell-cell interactions in the neuro-glial-vascular unit, thereby causing damage to adjacent brain tissue. Endothelial cells in SVD may become dysfunctional through intrinsic mechanisms via genetic vulnerability to SVD and/or via extrinsic factors such as hypertension, smoking and diabetes. Drugs that act on endothelial pathways are already looking promising in clinical trials, and understanding their action on endothelial cells and the surrounding brain may lead to the development of other therapies to limit disease progression and improve outcomes for individuals with SVD.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Kremer, R., Williams, A., & Wardlaw, J. (2025). Endothelial cells as key players in cerebral small vessel disease. Nature reviews. Neuroscience. https://doi.org/10.1038/s41583-024-00892-0

Vancouver

Kremer R, Williams A, Wardlaw J. Endothelial cells as key players in cerebral small vessel disease. Nature reviews. Neuroscience. 2025. doi:10.1038/s41583-024-00892-0. PMID: 39743557.

BibTeX

@article{kremer2025-39743557,
  author  = {Kremer, Ronja and Williams, Anna and Wardlaw, Joanna},
  title   = {{Endothelial cells as key players in cerebral small vessel disease}},
  journal = {Nature reviews. Neuroscience},
  year    = {2025},
  doi     = {10.1038/s41583-024-00892-0},
  pmid    = {39743557},
  url     = {https://doi.org/10.1038/s41583-024-00892-0}
}

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How to read this study

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Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

However, these interventions have limited effects, a proportion of individuals with sporadic SVD do not have hypertension, and SVD shows strong familial and genetic underpinnings.
Here, we describe the increasing evidence that cerebral endothelial cell dysfunction is a key mechanism of SVD.
Dysfunctional endothelial cells can cause cerebral blood vessel dysfunction, alter blood-brain barrier integrity and interfere with cell-cell interactions in the neuro-glial-vascular unit, thereby causing damage to adjacent brain tissue.
Endothelial cells in SVD may become dysfunctional through intrinsic mechanisms via genetic vulnerability to SVD and/or via extrinsic factors such as hypertension, smoking and diabetes.
Drugs that act on endothelial pathways are already looking promising in clinical trials, and understanding their action on endothelial cells and the surrounding brain may lead to the development of other therapies to limit disease progression and improve outcomes for individuals with SVD.

Study details

Evidence strengthLow

How this study scored 43/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multicenter collaboration and free to read, so those were left out: it earned 24 of the 56 points we could judge it on, which is 43 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Nature reviews. Neuroscience)
Journal's citation record	— / 4	No journal record from OpenAlex — left out of this score
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	4 / 5	2025 — within 3 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	— / 7	No citation count (not found in OpenAlex) — left out of this score
Citations per year	— / 5	No citation count or no year — left out of this score
Impact for its field and year	— / 6	No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here	— / 6	Not yet checked against this library's citation graph — left out of this score
Still being cited	— / 4	No yearly citation counts — left out of this score
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multicenter collaboration	— / 3	Institutions not listed — left out of this score
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 39743557)
Free to read	— / 2	Access not recorded — left out of this score
Points	24 / 56	Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100.
Total	43 / 100	—

What each of these 20 components measures, and what this score is not →

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