Seol, YunHee Ki, Soomin Ryu, Hannah L. Chung, Sooyoung Lee, Junghee Ryu, Hoon 2024-01-19T16:03:34Z 2024-01-19T16:03:34Z 2021-09-02 2020-11-17 1662-5099 https://pubs.kist.re.kr/handle/201004/117841 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. English FRONTIERS MEDIA SA UNFOLDED PROTEIN RESPONSE AMYLOID-BETA ALZHEIMERS-DISEASE ER STRESS MOLECULAR-MECHANISMS ACCUMULATION CLEARANCE ACTIVATION PEPTIDE PATHWAY How Microglia Manages Non-cell Autonomous Vicious Cycling of A beta Toxicity in the Pathogenesis of AD Article 10.3389/fnmol.2020.593724 1 FRONTIERS IN MOLECULAR NEUROSCIENCE, v.13 FRONTIERS IN MOLECULAR NEUROSCIENCE 13 scie scopus 000594382100001 2-s2.0-85097195895 Neurosciences Neurosciences & Neurology Review UNFOLDED PROTEIN RESPONSE AMYLOID-BETA ALZHEIMERS-DISEASE ER STRESS MOLECULAR-MECHANISMS ACCUMULATION CLEARANCE ACTIVATION PEPTIDE PATHWAY Alzheimer&#8217 s disease microglia amyloid-&#946 non-cell-autonomous toxicity vicious cycle