NDLI: A Study on the Pathogenesis of Vascular Cognitive Impairment and Dementia: The Chronic Cerebral Hypoperfusion Hypothesis

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A Study on the Pathogenesis of Vascular Cognitive Impairment and Dementia: The Chronic Cerebral Hypoperfusion Hypothesis

Content Provider	MDPI
Author	Yu, Weiwei Li, Yao Hu, Jun Wu, Jun Huang, Yining
Copyright Year	2022
Description	The pathogenic mechanisms underlying vascular cognitive impairment and dementia (VCID) remain controversial due to the heterogeneity of vascular causes and complexity of disease neuropathology. However, one common feature shared among all these vascular causes is cerebral blood flow (CBF) dysregulation, and chronic cerebral hypoperfusion (CCH) is the universal consequence of CBF dysregulation, which subsequently results in an insufficient blood supply to the brain, ultimately contributing to VCID. The purpose of this comprehensive review is to emphasize the important contributions of CCH to VCID and illustrate the current findings about the mechanisms involved in CCH-induced VCID pathological changes. Specifically, evidence is mainly provided to support the molecular mechanisms, including Aβ accumulation, inflammation, oxidative stress, blood-brain barrier (BBB) disruption, trophic uncoupling and white matter lesions (WMLs). Notably, there are close interactions among these multiple mechanisms, and further research is necessary to elucidate the hitherto unsolved questions regarding these interactions. An enhanced understanding of the pathological features in preclinical models could provide a theoretical basis, ultimately achieving the shift from treatment to prevention.
Starting Page	4742
e-ISSN	20770383
DOI	10.3390/jcm11164742
Journal	Journal of clinical medicine
Issue Number	16
Volume Number	11
Language	English
Publisher	MDPI
Publisher Date	2022-08-14
Access Restriction	Open
Subject Keyword	Journal of clinical medicine Journal of Clinical Medicine Hematology Vascular Cognitive Impairment and Dementia Cerebral Blood Flow Regulation Chronic Cerebral Hypoperfusion Β-amyloid Neuroinflammation Oxidative Stress Trophic Uncoupling Blood-brain Barrier White Matter Lesions
Content Type	Text
Resource Type	Article

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