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Emerging perspectives on mitochondrial dysfunction and inflammation in Alzheimer’s disease

BMB Reports 2020년 53권 1호 p.35 ~ 46
유승민 ( Yoo Seung-Min ) - Seoul National University School of Biological Sciences

 ( Park Ji-Su ) - Seoul National University School of Biological Sciences
 ( Kim Seo-Hyun ) - Seoul National University School of Biological Sciences
 ( Jung Yong-Keun ) - Seoul National University School of Biological Sciences

Abstract


Despite enduring diverse insults, mitochondria maintain normal functions through mitochondrial quality control. However, the failure of mitochondrial quality control resulting from excess damage and mechanical defects causes mitochondrial dysfunction, leading to various human diseases. Recent studies have reported that mitochondrial defects are found in Alzheimer’s disease (AD) and worsen AD symptoms. In AD pathogenesis, mitochondrial dysfunction-driven generation of reactive oxygen species (ROS) and their contribution to neuronal damage has been widely studied. In contrast, studies on mitochondrial dysfunction-associated inflammatory responses have been relatively scarce. Moreover, ROS produced upon failure of mitochondrial quality control may be linked to the inflammatory response and influence the progression of AD. Thus, this review will focus on inflammatory pathways that are associated with and initiated through defective mitochondria and will summarize recent progress on the role of mitochondria-mediated inflammation in AD. We will also discuss how reducing mitochondrial dysfunction-mediated inflammation could affect AD.

키워드

Alzheimer's disease; Dysfunction; Inflammation; Mitochondria
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