Blood-brain barrier endothelial cells in neurodegenerative diseases: Signals from the "barrier"

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 mechanism...

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Published inFrontiers in neuroscience Vol. 17; p. 1047778
Main Authors Yuan, Yiwen, Sun, Jian, Dong, Qiang, Cui, Mei
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 24.02.2023
Frontiers Media S.A
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Summary: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.
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Reviewed by: Mehmet Kaya, Koç University, Türkiye; Kosman Daniel, University at Buffalo, United States
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
These authors have contributed equally to this work
Edited by: Giuseppe Barisano, Stanford University, United States
ISSN:1662-4548
1662-453X
1662-453X
DOI:10.3389/fnins.2023.1047778