期刊
FRONTIERS IN NEUROSCIENCE
卷 17, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2023.1047778
关键词
blood-brain barrier; endothelial cells; neurovascular unit; neurodegenerative disease; Alzheimer's disease; Parkinson's disease
As blood-brain barrier (BBB) disruption becomes a common problem in early stages of neurodegenerative diseases, the crucial roles of barrier-type brain endothelial cells (BECs) in the pathophysiology of these diseases are being recognized. The mechanisms of how early vascular dysfunction contributes to neurodegeneration are still unclear, and understanding BEC functions is a promising start. This review presents current evidence of BEC dysfunction in neurodegenerative diseases and explores how BEC signals participate in the pathogenesis of these diseases.
As blood-brain barrier (BBB) disruption emerges as a common problem in the early stages of neurodegenerative diseases, the crucial roles of barrier-type brain endothelial cells (BECs), the primary part of the BBB, have been reported in the pathophysiology of neurodegenerative diseases. The mechanisms of how early vascular dysfunction contributes to the progress of neurodegeneration are still unclear, and understanding BEC functions is a promising start. Our understanding of the BBB has gone through different stages, from a passive diffusion barrier to a mediator of central-peripheral interactions. BECs serve two seemingly paradoxical roles: as a barrier to protect the delicate brain from toxins and as an interface to constantly receive and release signals, thus maintaining and regulating the homeostasis of the brain. Most previous studies about neurodegenerative diseases focus on the loss of barrier functions, and far too little attention has been paid to the active regulations of BECs. In this review, we present the current evidence of BEC dysfunction in neurodegenerative diseases and explore how BEC signals participate in the pathogenesis of neurodegenerative diseases.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据