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Vascular Dementia: From Pathophysiology to Therapeutic Frontiers
Han‐Mo Yang. Journal of Clinical Medicine, 2025-09-19
Topic: Risk, prevention and care in population studies
Vascular dementia (VaD) represents the second-most common dementia type after Alzheimer's disease since it results from complications of cerebrovascular disease. Mixed pathologies combining vascular and neurodegenerative processes are the rule rather than exception in elderly dementia patients. The condition known as VaD includes various types of vascular damage that affect both large and small blood vessels in the brain which results in cerebral hypoperfusion, blood-brain barrier disruption, glymphatic dysfunction, and molecular cascades causing neuronal damage. The mechanisms of VaD include endothelial dysfunction, oxidative stress, chronic neuroinflammation, impaired glymphatic clearance, white matter demyelination, and synaptic failure. The disease susceptibility of individuals depends on genetic factors which include NOTCH3 mutations and vascular risk polymorphisms. The diagnostic field uses neuroimaging tools and fluid biomarkers such as neurofilament light chain, inflammatory markers, and Aβ/tau ratios for mixed pathology. The current practice of vascular risk management combines with new therapeutic approaches that use phosphodiesterase inhibitors for cerebral perfusion and NLRP3 inflammasome inhibitors for neuroinflammation, senolytics for cellular senescence, and remyelination agents for white matter repair. However, the majority of new treatment methods remain investigational with limited Phase III data. Future medical treatment development will depend on precision medicine approaches which use biomarker-guided treatment selection and combination strategies targeting multiple pathological mechanisms.
Key findings
- Vascular dementia (VaD) represents the second-most common dementia type after Alzheimer's disease since it results from complications of cerebrovascular disease.
- The condition known as VaD includes various types of vascular damage that affect both large and small blood vessels in the brain which results in cerebral hypoperfusion, blood-brain barrier disruption, glymphatic dysfunction, and molecular cascades causing neuronal damage.
Why it matters
This review describes mechanisms of vascular dementia and notes that most new treatment approaches remain investigational. It concerns vascular dementia rather than Alzheimer's disease and reports no established treatment, cure or prevention.
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 (Journal of Clinical Medicine) |
| Journal's citation record | 2 / 4 | Journal of Clinical Medicine: journal h-index 188 (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 36 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.0 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 4 / 6 | Cited 11.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 36 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Han‐Mo Yang: h-index 37 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Seoul National University: institution h-index 1,053 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 41010812) |
| Free to read | 2 / 2 | Free to read |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3390/jcm14186611
- PubMed: 41010812
- Original source →
- Free full text: Journal of Clinical Medicine →
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. Check the citation against the original before you use it.
APA 7th
Yang, H. (2025). Vascular Dementia: From Pathophysiology to Therapeutic Frontiers. Journal of Clinical Medicine. https://doi.org/10.3390/jcm14186611
Vancouver
Yang H. Vascular Dementia: From Pathophysiology to Therapeutic Frontiers. Journal of Clinical Medicine. 2025. doi:10.3390/jcm14186611. PMID: 41010812.
BibTeX
@article{yang2025-41010812,
author = {Yang, Han‐Mo},
title = {{Vascular Dementia: From Pathophysiology to Therapeutic Frontiers}},
journal = {Journal of Clinical Medicine},
year = {2025},
doi = {10.3390/jcm14186611},
pmid = {41010812},
url = {https://doi.org/10.3390/jcm14186611}
}
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