Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer's Disease

被引:6
作者
Wu, Yi-Hsuan [1 ]
Hsieh, Hsi-Lung [1 ,2 ,3 ]
机构
[1] Chang Gung Univ Sci & Technol, Coll Human Ecol, Res Ctr Chinese Herbal Med, Taoyuan 333, Taiwan
[2] Chang Gung Univ Sci & Technol, Grad Inst Hlth Ind Technol, Dept Nursing, Div Basic Med Sci, Taoyuan 333, Taiwan
[3] Chang Gung Mem Hosp, Dept Neurol, Taoyuan 333, Taiwan
关键词
Alzheimer's disease; tau; beta-amyloid; APOE4; redox homeostasis; mitochondrial dysfunctions; INDUCED OXIDATIVE STRESS; AMYLOID-BETA; MOUSE MODEL; VITAMIN-E; NEURODEGENERATIVE DISEASES; A-BETA; NEUROFIBRILLARY TANGLES; TARGETED ANTIOXIDANT; COGNITIVE IMPAIRMENT; SYNAPTIC DYSFUNCTION;
D O I
10.3390/antiox12101816
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Bioenergetic mitochondrial dysfunction is a common feature of several diseases, including Alzheimer's disease (AD), where redox imbalance also plays an important role in terms of disease development. AD is an age-related disease and begins many years before the appearance of neurodegenerative symptoms. Intracellular tau aggregation, extracellular beta-amyloid (A beta) deposition in the brain, and even the APOE4 genotype contribute to the process of AD by impairing redox homeostasis and mitochondrial dysfunction. This review summarizes the evidence for the redox imbalance and mitochondrial dysfunction in AD and demonstrates the current therapeutic strategies related to mitochondrial maintenance.
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页数:18
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