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45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Digital health tools

Topic: Risk, prevention and care in population studies

Vascular dementia (VaD) is the second most common type of dementia after Alzheimer's disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable. CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood-brain barrier damage, followed by the activation of glia and inflammatory environment in the brain. White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment. The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD. Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD.

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

APA 7th

Wang, F., Cao, Y., Ma, L., Pei, H., Rausch, W. D., & Li, H. (2018). Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2018.00376

Vancouver

Wang F, Cao Y, Ma L, Pei H, Rausch WD, Li H. Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia. Frontiers in aging neuroscience. 2018. doi:10.3389/fnagi.2018.00376. PMID: 30505270.

BibTeX

@article{wang2018-30505270,
  author  = {Wang, F. and Cao, Y. and Ma, L. and Pei, H. and Rausch, W. D. and Li, H.},
  title   = {{Dysfunction of Cerebrovascular Endothelial Cells: Prelude to Vascular Dementia}},
  journal = {Frontiers in aging neuroscience},
  year    = {2018},
  doi     = {10.3389/fnagi.2018.00376},
  pmid    = {30505270},
  url     = {https://doi.org/10.3389/fnagi.2018.00376}
}

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Key findings

VaD is usually caused by cerebrovascular disease, during which, cerebrovascular endothelial cells (CECs) are vulnerable.
CEC dysfunction occurs before the onset of VaD and can eventually lead to dysregulation of cerebral blood flow and blood-brain barrier damage, followed by the activation of glia and inflammatory environment in the brain.
White matter, neuronal axons, and synapses are compromised in this process, leading to cognitive impairment.
The present review summarizes the mechanisms underlying CEC impairment during hypoperfusion and pathological role of CECs in VaD.
Through the comprehensive examination and summarization, endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway, Ras homolog gene family member A (RhoA) signaling pathway, and CEC-derived caveolin-1 (CAV-1) are proposed to serve as targets of new drugs for the treatment of VaD.

Why it matters

This review proposes that dysfunction of cerebrovascular endothelial cells occurs before vascular dementia and suggests eNOS/NO, RhoA, and caveolin-1 as targets for new drugs. These are proposed targets only, not tested treatments, and the focus is vascular dementia rather than Alzheimer's disease.

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Study details

Evidence strengthLow

How this study scored 45/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience)
Journal's citation record	2 / 4	Frontiers in Aging Neuroscience: journal h-index 174 (OpenAlex, 2026-10-29)
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	2 / 5	2018 — within 10 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)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 157 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	15.7 citations a year over 10 year(s) since 2018
Impact for its field and year	3 / 6	Cited 5.3× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 4 other studies in this library
Still being cited	3 / 4	Cited 54 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Hao Li: h-index 38 (OpenAlex, whole career)
Institution's track record	0 / 3	China Academy of Chinese Medical Sciences: institution h-index 304 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 30505270)
Free to read	2 / 2	Free to read
Total	45 / 100	—

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