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Chronic cerebral hypoperfusion: a key mechanism leading to vascular cognitive impairment and dementia. Closing the translational gap between rodent models and human vascular cognitive impairment and dementia
Duncombe J, Kitamura A, Hase Y, Ihara M, Kalaria RN, Horsburgh K.. Clinical science (London, England : 1979), 2017-09-28
Topic: Brain proteins, microglia and lab models
Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia. While there is considerable overlap between features of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD), it appears that cerebral hypoperfusion is the common underlying pathophysiological mechanism which is a major contributor to cognitive decline and degenerative processes leading to dementia. Sustained cerebral hypoperfusion is suggested to be the cause of white matter attenuation, a key feature common to both AD and dementia associated with cerebral small vessel disease (SVD). White matter changes increase the risk for stroke, dementia and disability. A major gap has been the lack of mechanistic insights into the evolution and progress of VCID. However, this gap is closing with the recent refinement of rodent models which replicate chronic cerebral hypoperfusion. In this review, we discuss the relevance and advantages of these models in elucidating the pathogenesis of VCID and explore the interplay between hypoperfusion and the deposition of amyloid β (Aβ) protein, as it relates to AD. We use examples of our recent investigations to illustrate the utility of the model in preclinical testing of candidate drugs and lifestyle factors. We propose that the use of such models is necessary for tackling the urgently needed translational gap from preclinical models to clinical treatments.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Duncombe, J., Kitamura, A., Hase, Y., Ihara, M., Kalaria, R. N., & Horsburgh, K. (2017). Chronic cerebral hypoperfusion: a key mechanism leading to vascular cognitive impairment and dementia. Closing the translational gap between rodent models and human vascular cognitive impairment and dementia. Clinical science (London, England : 1979). https://doi.org/10.1042/cs20160727
Vancouver
Duncombe J, Kitamura A, Hase Y, Ihara M, Kalaria RN, Horsburgh K. Chronic cerebral hypoperfusion: a key mechanism leading to vascular cognitive impairment and dementia. Closing the translational gap between rodent models and human vascular cognitive impairment and dementia. Clinical science (London, England : 1979). 2017. doi:10.1042/cs20160727. PMID: 28963120.
BibTeX
@article{duncombe2017-28963120,
author = {Duncombe, J. and Kitamura, A. and Hase, Y. and Ihara, M. and Kalaria, R. N. and Horsburgh, K.},
title = {{Chronic cerebral hypoperfusion: a key mechanism leading to vascular cognitive impairment and dementia. Closing the translational gap between rodent models and human vascular cognitive impairment and dementia}},
journal = {Clinical science (London, England : 1979)},
year = {2017},
doi = {10.1042/cs20160727},
pmid = {28963120},
url = {https://doi.org/10.1042/cs20160727}
}
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Key findings
- Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia.
- Sustained cerebral hypoperfusion is suggested to be the cause of white matter attenuation, a key feature common to both AD and dementia associated with cerebral small vessel disease (SVD).
Why it matters
This review argues that sustained reduced blood flow to the brain may cause white matter damage, a feature shared by Alzheimer's disease and small vessel disease. It proposes that refined rodent models of chronic cerebral hypoperfusion are needed to test candidate drugs and lifestyle factors before human trials.
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Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Clinical science (London, England : 1979)) |
| Journal's citation record | 2 / 4 | Clinical Science: journal h-index 212 (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 | 2017 — 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 | Laboratory or animal study (title names “rodent”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 405 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 36.8 citations a year over 11 year(s) since 2017 |
| Impact for its field and year | 4 / 6 | Cited 10.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 8 other studies in this library |
| Still being cited | 3 / 4 | Cited 143 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Karen J. Horsburgh: h-index 46 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Edinburgh: institution h-index 1,378 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 28963120) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
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Read the original
- DOI: 10.1042/cs20160727
- PubMed: 28963120
- Original source →
- Free full text: Edinburgh Research Explorer (University of Edinburgh) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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