期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 483, 期 4, 页码 1020-1030出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.08.153
关键词
Parkinson disease; Mitochondria; Calcium; Dopaminergic neurons; PD-related proteins
资金
- Ministry of University and Research (Bando SIR) [RBSI14C65Z]
- University of Padova (Progetto Giovani) [GRIC128SP0]
- University of Padova (Progetto di Ateneo) [CPDA153402]
The selective cell loss in the ventral component of the substantia nigra pars compacta and the presence of alpha-synuclein (alpha-syn)-rich intraneuronal inclusions called Lewy bodies are the pathological hallmarks of Parkinson's disease (PD), the most common motor system disorder whose aetiology remains largely elusive. Although most cases of PD are idiopathic, there are rare familial forms of the disease that can be traced to single gene mutations that follow Mendelian inheritance pattern. The study of several nuclear encoded proteins whose mutations are linked to the development of autosomal recessive and dominant forms of familial PD enhanced our understanding of biochemical and cellular mechanisms contributing to the disease and suggested that many signs of neurodegeneration result from compromised mitochondrial function. Here we present an overview of the current understanding of PD-related mitochondrial dysfunction including defects in bioenergetics and Ca2+ homeostasis, mitochondrial DNA mutations, altered mitochondria! dynamics and autophagy. We emphasize, in particular, the convergence of many apparently different pathways towards a common route involving mitochondria. Understanding whether mitochondrial dysfunction in PD represents the cause or the consequence of the disease is challenging and will help to define the pathogenic processes at the basis of the PD onset and progression. (C) 2016 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据