Home › Research › Prevention trials
Cerebromicrovascular senescence in vascular cognitive impairment: does accelerated microvascular aging accompany atherosclerosis?
Anna Ungvari, Ádám Nyúl‐Tóth, Roland Patai, Boglárka Csík, Rafał Gulej, Dorina Nagy, Santny Shanmugarama, Zoltán Benyó et al.. GeroScience, 2025-03-21
Topic: Risk, prevention and care in population studies
Vascular cognitive impairment (VCI) is a leading cause of age-related cognitive decline, driven by cerebrovascular dysfunction and cerebral small vessel disease (CSVD). Emerging evidence suggests that cerebromicrovascular endothelial senescence plays an important role in the pathogenesis of VCI by promoting cerebral blood flow dysregulation, neurovascular uncoupling, blood-brain barrier (BBB) disruption, and the development of cerebral microhemorrhages (CMHs). This review explores the concept of cerebromicrovascular senescence as a continuum of vascular aging, linking macrovascular atherosclerosis with microvascular dysfunction. It examines the mechanisms by which endothelial senescence drives neurovascular pathology and highlights the impact of cardiovascular risk factors in accelerating these processes. We examine preclinical and clinical studies that provide compelling evidence that atherosclerosis-induced microvascular senescence exacerbates cognitive impairment. In particular, findings suggest that targeting senescent endothelial cells through senolytic therapy can restore cerebrovascular function and improve cognitive outcomes in experimental models of atherosclerosis. Given the growing recognition of microvascular senescence as a therapeutic target, further research is warranted to explore novel interventions such as senolytics, anti-inflammatory agents, and metabolic modulators. The development of circulating biomarkers of vascular senescence (e.g., senescence-associated secretory phenotype [SASP] components and endothelial-derived extracellular vesicles) could enable early detection and risk stratification in individuals at high risk for VCI. Additionally, lifestyle modifications, including the Mediterranean diet, hold promise for delaying endothelial senescence and mitigating cognitive decline. In conclusion, cerebromicrovascular senescence is a key mechanistic link between atherosclerosis and cognitive impairment. Addressing microvascular aging as a modifiable risk factor through targeted interventions offers a promising strategy for reducing the burden of VCI and preserving cognitive function in aging populations.
Key findings
- Emerging evidence suggests that cerebromicrovascular endothelial senescence plays an important role in the pathogenesis of VCI by promoting cerebral blood flow dysregulation, neurovascular uncoupling, blood-brain barrier (BBB) disruption, and the development of cerebral microhemorrhages (CMHs).
- In particular, findings suggest that targeting senescent endothelial cells through senolytic therapy can restore cerebrovascular function and improve cognitive outcomes in experimental models of atherosclerosis.
- In conclusion, cerebromicrovascular senescence is a key mechanistic link between atherosclerosis and cognitive impairment.
Why it matters
This review describes how cerebromicrovascular endothelial senescence may contribute to vascular cognitive impairment by disrupting cerebral blood flow, neurovascular coupling, the blood-brain barrier, and by promoting cerebral microhemorrhages. It notes that targeting senescent endothelial cells with senolytic therapy restored cerebrovascular function and improved cognitive outcomes in experimental models of atherosclerosis, so this is preclinical evidence, not a proven treatment for people.
New to this subject? Start with our plain-English guide: Prevention →
Study details
- Evidence strengthLow
How this study scored 46/100
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 (GeroScience) |
| Journal's citation record | 1 / 4 | GeroScience: journal h-index 83 (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 | 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 24 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 7.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 2 / 4 | Cited 24 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Anna Csiszár: h-index 98 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Oklahoma: institution h-index 716 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40113668) |
| Free to read | 2 / 2 | Free to read |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Ungvari, A., Nyúl‐Tóth, Á., Patai, R., Csík, B., Gulej, R., Nagy, D., et al. (2025). Cerebromicrovascular senescence in vascular cognitive impairment: does accelerated microvascular aging accompany atherosclerosis? GeroScience. https://doi.org/10.1007/s11357-025-01621-w
Vancouver
Ungvari A, Nyúl‐Tóth Á, Patai R, Csík B, Gulej R, Nagy D, et al. Cerebromicrovascular senescence in vascular cognitive impairment: does accelerated microvascular aging accompany atherosclerosis? GeroScience. 2025. doi:10.1007/s11357-025-01621-w. PMID: 40113668.
BibTeX
@article{ungvari2025-40113668,
author = {Ungvari, Anna and Nyúl‐Tóth, Ádám and Patai, Roland and Csík, Boglárka and Gulej, Rafał and Nagy, Dorina and Shanmugarama, Santny and Benyó, Zoltán and others},
title = {{Cerebromicrovascular senescence in vascular cognitive impairment: does accelerated microvascular aging accompany atherosclerosis?}},
journal = {GeroScience},
year = {2025},
doi = {10.1007/s11357-025-01621-w},
pmid = {40113668},
url = {https://doi.org/10.1007/s11357-025-01621-w}
}
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
Later studies that cite this one
3 studies in the alzhub library list this one in their references.