Journal
FRONTIERS IN MOLECULAR NEUROSCIENCE
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fnmol.2020.593724
Keywords
Alzheimer’ s disease; microglia; amyloid-β non-cell-autonomous toxicity; vicious cycle
Categories
Funding
- National Research Foundation of Korea from the Ministry of Science, ICT and Future Planning [NRF-2016M3C7A1904233, NRF-2018M3C7A1056894, NRF-2020M3E5D9079742]
- National Research Council of Science and Technology (NST) Grant from the Korea government (MSIP) [CRC-15-04-KIST]
- Korea Institute of Science and Technology [2E30320, 2E30762]
- NIH [NS109537, AG054156]
- National Research Foundation of Korea [2016M3C7A1904233] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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.
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