Mitochondrial abnormalities in Parkinson's disease and Alzheimer's disease: can mitochondria be targeted therapeutically?

被引：132
|
作者：
Macdonald, Ruby [1 ]
Barnes, Katy [1 ]
Hastings, Christopher [1 ]
Mortiboys, Heather [1 ]
机构：
[1] Univ Sheffield, Sheffield Inst Translat Neurosci SITraN, 385a Glossop Rd, Sheffield S10 2HQ, S Yorkshire, England
来源：
BIOCHEMICAL SOCIETY TRANSACTIONS | 2018年 / 46卷
关键词：
COMPLEX-I DEFICIENCY; CYTOCHROME-C-OXIDASE; TRANSGENIC MOUSE MODEL; DEEP BRAIN-STIMULATION; AMYLOID-BETA; OXIDATIVE STRESS; SPORADIC PARKINSONS; SUBSTANTIA-NIGRA; DNA DELETIONS; ANTIOXIDANT MITOQ;
D O I：
10.1042/BST20170501
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：
Mitochondrial abnormalities have been identified as a central mechanism in multiple neurodegenerative diseases and, therefore, the mitochondria have been explored as a therapeutic target. This review will focus on the evidence for mitochondrial abnormalities in the two most common neurodegenerative diseases, Parkinson's disease and Alzheimer's disease. In addition, we discuss the main strategies which have been explored in these diseases to target the mitochondria for therapeutic purposes, focusing on mitochondrially targeted antioxidants, peptides, modulators of mitochondrial dynamics and phenotypic screening outcomes.
引用
收藏
页码：891 / 909
页数：19
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