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Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease
Inoue Y, Shue F, Bu G, Kanekiyo T.. Molecular neurodegeneration, 2023-07-11
Topic: Amyloid, tau and blood-test diagnosis
Vascular cognitive impairment and dementia (VCID) is commonly caused by vascular injuries in cerebral large and small vessels and is a key driver of age-related cognitive decline. Severe VCID includes post-stroke dementia, subcortical ischemic vascular dementia, multi-infarct dementia, and mixed dementia. While VCID is acknowledged as the second most common form of dementia after Alzheimer's disease (AD) accounting for 20% of dementia cases, VCID and AD frequently coexist. In VCID, cerebral small vessel disease (cSVD) often affects arterioles, capillaries, and venules, where arteriolosclerosis and cerebral amyloid angiopathy (CAA) are major pathologies. White matter hyperintensities, recent small subcortical infarcts, lacunes of presumed vascular origin, enlarged perivascular space, microbleeds, and brain atrophy are neuroimaging hallmarks of cSVD. The current primary approach to cSVD treatment is to control vascular risk factors such as hypertension, dyslipidemia, diabetes, and smoking. However, causal therapeutic strategies have not been established partly due to the heterogeneous pathogenesis of cSVD. In this review, we summarize the pathophysiology of cSVD and discuss the probable etiological pathways by focusing on hypoperfusion/hypoxia, blood-brain barriers (BBB) dysregulation, brain fluid drainage disturbances, and vascular inflammation to define potential diagnostic and therapeutic targets for cSVD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Inoue, Y., Shue, F., Bu, G., & Kanekiyo, T. (2023). Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease. Molecular neurodegeneration. https://doi.org/10.1186/s13024-023-00640-5
Vancouver
Inoue Y, Shue F, Bu G, Kanekiyo T. Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease. Molecular neurodegeneration. 2023. doi:10.1186/s13024-023-00640-5. PMID: 37434208.
BibTeX
@article{inoue2023-37434208,
author = {Inoue, Y. and Shue, F. and Bu, G. and Kanekiyo, T.},
title = {{Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease}},
journal = {Molecular neurodegeneration},
year = {2023},
doi = {10.1186/s13024-023-00640-5},
pmid = {37434208},
url = {https://doi.org/10.1186/s13024-023-00640-5}
}
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.
Key findings
- In VCID, cerebral small vessel disease (cSVD) often affects arterioles, capillaries, and venules, where arteriolosclerosis and cerebral amyloid angiopathy (CAA) are major pathologies.
- White matter hyperintensities, recent small subcortical infarcts, lacunes of presumed vascular origin, enlarged perivascular space, microbleeds, and brain atrophy are neuroimaging hallmarks of cSVD.
- The current primary approach to cSVD treatment is to control vascular risk factors such as hypertension, dyslipidemia, diabetes, and smoking.
- However, causal therapeutic strategies have not been established partly due to the heterogeneous pathogenesis of cSVD.
- In this review, we summarize the pathophysiology of cSVD and discuss the probable etiological pathways by focusing on hypoperfusion/hypoxia, blood-brain barriers (BBB) dysregulation, brain fluid drainage disturbances, and vascular inflammation to define potential diagnostic and therapeutic targets for cSVD.
Why it matters
This review describes cerebral small vessel disease as a common cause of vascular cognitive impairment and dementia, which frequently coexists with Alzheimer's disease. It states that the current main approach is to control vascular risk factors such as hypertension, dyslipidemia, diabetes, and smoking, and that causal therapeutic strategies have not been established.
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Study details
- Evidence strengthLow
How this study scored 56/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (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 | 3 / 5 | 2023 — within 6 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 | 6 / 7 | Cited 329 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 65.8 citations a year over 5 year(s) since 2023 |
| Impact for its field and year | 5 / 6 | Cited 27.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 22 other studies in this library |
| Still being cited | 4 / 4 | Cited 321 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Takahisa Kanekiyo: h-index 59 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 37434208) |
| Free to read | 2 / 2 | Free to read |
| Total | 56 / 100 | — |
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Read the original
- DOI: 10.1186/s13024-023-00640-5
- PubMed: 37434208
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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