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Cerebrovascular p16 INK4A expression induces cerebral small vessel disease-related phenotypes
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Cerebrovascular p16 INK4A expression induces cerebral small vessel disease-related phenotypes
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Journal Article
Cerebrovascular p16 INK4A expression induces cerebral small vessel disease-related phenotypes
2025
Overview
Cerebral small vessel disease (cSVD) is the most common cause of vascular cognitive impairment and dementia (VCID) and highly associated with Alzheimer's disease pathogenesis. There is an urgent need to establish relevant animal models for cSVD. As aging is the strongest risk factor for these diseases, cerebrovascular senescence is implicated in cSVD pathogenesis. We investigated how AAV-based expression of senescence marker CDKN2A/p16
in cerebrovascular endothelial cells influences cSVD phenotypes in adult wild-type mice. A single intraperitoneal injection of the AAV carrying CDKN2A/p16
caused blood-brain barrier impairments, neurovascular uncoupling, and reduction of cerebral blood flow, accompanied with behavioral changes in mice. While single cell RNA-sequencing and immunostaining revealed the upregulation of VCAM1 in cerebrovascular endothelial cells, in vivo two-photon excitation microscopy detected aggravated leukocyte adhesions to capillaries. Our findings demonstrate the contributions of p16
in cerebrovascular endothelial cells to cSVD and VCID pathogenesis through new mouse model.
Subject
/ Blood-Brain Barrier - metabolism
/ Blood-Brain Barrier - pathology
/ Cerebral Small Vessel Diseases - genetics
/ Cerebral Small Vessel Diseases - metabolism
/ Cerebral Small Vessel Diseases - pathology
/ Cerebrovascular Circulation - physiology
/ Cyclin-Dependent Kinase Inhibitor p16 - genetics
/ Cyclin-Dependent Kinase Inhibitor p16 - metabolism
/ Endothelial Cells - metabolism
/ Endothelial Cells - pathology
/ Male
/ Mice
