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Department of Brain Sciences
Laboratory of Neurodegenerative Diseases and Aging
1. Journal Articles
Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson's Disease Treatment
Lee, Davin
;
Jo, Min Gu
;
Kim, Seung Yeon
;
Chung, Chang Geon
;
Lee, Sung Bae
Department of Brain Sciences
Laboratory of Neurodegenerative Diseases and Aging
1. Journal Articles
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Title
Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson's Disease Treatment
Issued Date
2020-11
Citation
Lee, Davin. (2020-11). Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson's Disease Treatment. Antioxidants, 9(11), 1056–22. doi: 10.3390/antiox9111056
Type
Article
Author Keywords
dietary antioxidants
;
mitochondria
;
reactive oxygen species
;
neurodegenerative disease
;
Parkinson’
;
s disease
;
mitochondrial quality control
Keywords
AGING-RELATED CHANGES
;
OXIDATIVE STRESS
;
MOLECULAR-MECHANISMS
;
VITAMIN-E
;
DOPAMINERGIC-NEURONS
;
TEA POLYPHENOL
;
RAT MODEL
;
IN-VITRO
;
DYSFUNCTION
;
CELL
ISSN
2076-3921
Abstract
Advances in medicine and dietary standards over recent decades have remarkably increased human life expectancy. Unfortunately, the chance of developing age‐related diseases, including neurodegenerative diseases (NDDs), increases with increased life expectancy. High metabolic demands of neurons are met by mitochondria, damage of which is thought to contribute to the development of many NDDs including Parkinson’s disease (PD). Mitochondrial damage is closely associated with the abnormal production of reactive oxygen species (ROS), which are widely known to be toxic in various cellular environments, including NDD contexts. Thus, ways to prevent or slow mitochondrial dysfunction are needed for the treatment of these NDDs. In this review, we first detail how ROS are associated with mitochondrial dysfunction and review the cellular mechanisms, such as the mitochondrial quality control (MQC) system, by which neurons defend against both abnormal production of ROS and the subsequent accumulation of damaged mitochondria. We next highlight previous studies that link mitochondrial dysfunction with PD and how dietary antioxidants might provide reinforcement of the MQC system. Finally, we discuss how aging plays a role in mitochondrial dysfunction and PD before considering how healthy aging through proper diet and exercise may be salutary. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
URI
http://hdl.handle.net/20.500.11750/12685
DOI
10.3390/antiox9111056
Publisher
MDPI AG
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Lee, Sung Bae
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Department of Brain Sciences
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