New insight into neurological degeneration: Inflammatory cytokines and blood–brain barrier
Neurological degeneration after neuroinflammation, such as that resulting from Alzheimer’s disease (AD), stroke, multiple sclerosis (MS), and post-traumatic brain injury (TBI), is typically associated with high mortality and morbidity and with permanent cognitive dysfunction, which places a heavy ec...
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Published in | Frontiers in molecular neuroscience Vol. 15; p. 1013933 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Lausanne
Frontiers Research Foundation
24.10.2022
Frontiers Media S.A |
Subjects | |
Online Access | Get full text |
ISSN | 1662-5099 1662-5099 |
DOI | 10.3389/fnmol.2022.1013933 |
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Summary: | Neurological degeneration after neuroinflammation, such as that resulting from Alzheimer’s disease (AD), stroke, multiple sclerosis (MS), and post-traumatic brain injury (TBI), is typically associated with high mortality and morbidity and with permanent cognitive dysfunction, which places a heavy economic burden on families and society. Diagnosing and curing these diseases in their early stages remains a challenge for clinical investigation and treatment. Recent insight into the onset and progression of these diseases highlights the permeability of the blood–brain barrier (BBB). The primary factor that influences BBB structure and function is inflammation, especially the main cytokines including IL-1β, TNFα, and IL-6, the mechanism on the disruption of which are critical component of the aforementioned diseases. Surprisingly, the main cytokines from systematic inflammation can also induce as much worse as from neurological diseases or injuries do. In this review, we will therefore discuss the physiological structure of BBB, the main cytokines including IL-1β, TNFα, IL-6, and their mechanism on the disruption of BBB and recent research about the main cytokines from systematic inflammation inducing the disruption of BBB and cognitive impairment, and we will eventually discuss the need to prevent the disruption of BBB. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 Reviewed by: Fumitaka Shimizu, Yamaguchi University, Japan; Nadine Ahmed Kerr, University of Miami, United States Edited by: Juan Pablo de Rivero Vaccari, University of Miami, United States These authors have contributed equally to this work This article was submitted to Brain Disease Mechanisms, a section of the journal Frontiers in Molecular Neuroscience |
ISSN: | 1662-5099 1662-5099 |
DOI: | 10.3389/fnmol.2022.1013933 |