How Microglia Manages Non-cell Autonomous Vicious Cycling of A beta Toxicity in the Pathogenesis of AD

Authors
Seol, YunHeeKi, SoominRyu, Hannah L.Chung, SooyoungLee, JungheeRyu, Hoon
Issue Date
2020-11-17
Publisher
FRONTIERS MEDIA SA
Citation
FRONTIERS IN MOLECULAR NEUROSCIENCE, v.13
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease and a common form of dementia that affects cognition and memory mostly in aged people. AD pathology is characterized by the accumulation of beta-amyloid (A beta) senile plaques and the neurofibrillary tangles of phosphorylated tau, resulting in cell damage and neurodegeneration. The extracellular deposition of A beta is regarded as an important pathological marker and a principal-agent of neurodegeneration. However, the exact mechanism of A beta-mediated pathogenesis is not fully understood yet. Recently, a growing body of evidence provides novel insights on the major role of microglia and its non-cell-autonomous cycling of A beta toxicity. Hence, this article provides a comprehensive overview of microglia as a significant player in uncovering the underlying disease mechanisms of AD.
Keywords
UNFOLDED PROTEIN RESPONSE; AMYLOID-BETA; ALZHEIMERS-DISEASE; ER STRESS; MOLECULAR-MECHANISMS; ACCUMULATION; CLEARANCE; ACTIVATION; PEPTIDE; PATHWAY; UNFOLDED PROTEIN RESPONSE; AMYLOID-BETA; ALZHEIMERS-DISEASE; ER STRESS; MOLECULAR-MECHANISMS; ACCUMULATION; CLEARANCE; ACTIVATION; PEPTIDE; PATHWAY; Alzheimer’ s disease; microglia; amyloid-β non-cell-autonomous toxicity; vicious cycle
ISSN
1662-5099
URI
https://pubs.kist.re.kr/handle/201004/117841
DOI
10.3389/fnmol.2020.593724
Appears in Collections:
KIST Article > 2020
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE