Journal
NEUROBIOLOGY OF DISEASE
Volume 170, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2022.105750
Keywords
Cerebral small vessel disease; Neurovascular unit; Microcirculation; Neuroimaging markers; Cognitive impairment
Categories
Funding
- National Natural Science Foundation of China [81901310]
- Guangdong Provincial Key Lab-oratory of Shock and Microcirculation, Initiated Foundation of Zhujiang Hospital [02020318005]
- Science and Technology Program of Guangdong of China [2020A0505100037]
- Leading Talent in Talents Project Guangdong High-level Personnel of Special Support Program
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Growing evidence suggests a significant association between altered neurovascular unit functioning and the pathophysiology of vascular cognitive impairment (VCI) caused by cerebral small vessel disease (CSVD). NVU dysregulation may lead to the entry of pathogens from the blood into the cerebral parenchyma by altering the blood-brain barrier (BBB), resulting in VCI. Additionally, the coupling of neural activity with cerebral blood flow and the clearance of metabolic byproducts may also be affected by NVU dysregulation.
Cerebral small vessel disease (CSVD) is a generic term used for intracranial vascular disorders caused by the structural changes of cerebral microvessels, including the small arteries, arterioles, capillaries and venules. CSVD exhibits various neuroimaging features and is associated clinical characteristics. Although CSVD is recognized as the leading cause of vascular cognitive impairment (VCI), the underlying mechanism(s) remains elusive. Growing evidence indicates a significant association between altered neurovascular unit (NVU) functioning and the pathophysiology of evolving CSVD-induced VCI. Therefore, research is required to understand how NVU dysregulation contributes to cognitive impairment due to CSVD. In this review, we describe the link between the neuroimaging focal lesions and cognitive alterations. We also discuss the potential pathological role of NVU dysregulation in the entry of pathogens from the blood into the parenchyma by altering the blood-brain barrier (BBB), affecting the cerebral microvascular and consequently cause VCI. Next, we review the coupling of neural activity with cerebral blood flow to control the microvascular perfusion; and the disrupted clearance of metabolic byproducts with CSF-ISF exchange via
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