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The pathobiology of vascular dementia
Iadecola C.. Neuron, 2013-11-01
Topic: Risk, prevention and care in population studies
Vascular cognitive impairment defines alterations in cognition, ranging from subtle deficits to full-blown dementia, attributable to cerebrovascular causes. Often coexisting with Alzheimer's disease, mixed vascular and neurodegenerative dementia has emerged as the leading cause of age-related cognitive impairment. Central to the disease mechanism is the crucial role that cerebral blood vessels play in brain health, not only for the delivery of oxygen and nutrients, but also for the trophic signaling that inextricably links the well-being of neurons and glia to that of cerebrovascular cells. This review will examine how vascular damage disrupts these vital homeostatic interactions, focusing on the hemispheric white matter, a region at heightened risk for vascular damage, and on the interplay between vascular factors and Alzheimer's disease. Finally, preventative and therapeutic prospects will be examined, highlighting the importance of midlife vascular risk factor control in the prevention of late-life dementia.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Iadecola, C. (2013). The pathobiology of vascular dementia. Neuron. https://doi.org/10.1016/j.neuron.2013.10.008
Vancouver
Iadecola C. The pathobiology of vascular dementia. Neuron. 2013. doi:10.1016/j.neuron.2013.10.008. PMID: 24267647.
BibTeX
@article{iadecola2013-24267647,
author = {Iadecola, C.},
title = {{The pathobiology of vascular dementia}},
journal = {Neuron},
year = {2013},
doi = {10.1016/j.neuron.2013.10.008},
pmid = {24267647},
url = {https://doi.org/10.1016/j.neuron.2013.10.008}
}
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Key findings
- Vascular cognitive impairment defines alterations in cognition, ranging from subtle deficits to full-blown dementia, attributable to cerebrovascular causes.
- Often coexisting with Alzheimer's disease, mixed vascular and neurodegenerative dementia has emerged as the leading cause of age-related cognitive impairment.
- Central to the disease mechanism is the crucial role that cerebral blood vessels play in brain health, not only for the delivery of oxygen and nutrients, but also for the trophic signaling that inextricably links the well-being of neurons and glia to that of cerebrovascular cells.
- This review will examine how vascular damage disrupts these vital homeostatic interactions, focusing on the hemispheric white matter, a region at heightened risk for vascular damage, and on the interplay between vascular factors and Alzheimer's disease.
- Finally, preventative and therapeutic prospects will be examined, highlighting the importance of midlife vascular risk factor control in the prevention of late-life dementia.
Why it matters
This narrative review defines vascular cognitive impairment as changes in thinking "attributable to cerebrovascular causes", from subtle deficits to dementia. It notes that vascular damage often coexists with Alzheimer's disease. It sets out to examine how damaged blood vessels disrupt their support of nerve and glial cells, especially in the brain's white matter, and it highlights "the importance of midlife vascular risk factor control in the prevention of late-life dementia." It is an expert review, not a trial, so that prevention point is the author's emphasis rather than a tested result.
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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 randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuron) |
| Journal's citation record | 4 / 4 | Neuron: journal h-index 689 (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 | 1 / 5 | 2013 — within 20 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 | 7 / 7 | Cited 1,852 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 123.5 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 6 / 6 | Cited 42.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 69 other studies in this library |
| Still being cited | 4 / 4 | Cited 511 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Costantino Iadecola: h-index 128 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Weill Cornell Medicine: institution h-index 1,163 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24267647) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 56 / 100 | — |
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Read the original
- DOI: 10.1016/j.neuron.2013.10.008
- PubMed: 24267647
- Original source →
- Free full text: PubMed Central →
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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