The DOI matches its Crossref record; 143 of the 143 references it cites were found in a registry or an index.
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
Open accessAbstract
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.
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Cited by
Vascular Cognitive Impairment and Dementia
Iadecola, C., Duering, M., Hachinski, V., Joutel, A., Pendlebury, S. T., Schneider, J. A., & Dichgans, M. (2019) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2019.04.034 · Cited by 801
Zhao, Y., Zhang, J., Zheng, Y., Zhang, Y., Zhang, X. J., Wang, H., Du, Y., Guan, J., Wang, X., & Fu, J. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02250-8 · Cited by 348
White matter capillaries in vascular and neurodegenerative dementias
Hase, Y., Ding, R., Harrison, G., Hawthorne, E., King, A., Gettings, S., Platten, C., Stevenson, W., Craggs, L. J. L., & Kalaria, R. N. (2019) · Acta Neuropathologica Communications · doi:10.1186/s40478-019-0666-x · Cited by 101
Self-citationAssociation of small vessel disease with tau pathology
Kapasi, A., Yu, L., Petyuk, V., Arfanakis, K., Bennett, D. A., & Schneider, J. A. (2022) · Acta Neuropathologica · doi:10.1007/s00401-021-02397-x · Cited by 55
Deng, Y., Zou, J., Hong, Y., Peng, Q., Fu, X., Duan, R., Chen, J., & Chen, X. (2022) · Cells · doi:10.3390/cells11223650 · Cited by 48
Metadata
- Authors
- Duncombe, J., Kitamura, A., Hase, Y., Ihara, M., Kalaria, R. N., & Horsburgh, K.
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2017-09-28
- Volume
- 131
- Issue
- 19
- Pages
- 2451-2468
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- OpenAlex
- W2758846139
- Cited by
- 401
- References
- 143
- FWCI
- 10.85
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: 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. https://app.cochat.ai/papers/10.1042/cs20160727
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- 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. https://doi.org/10.1042/cs20160727
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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