Document Detail


Mitochondrial dysfunction and biogenesis in the pathogenesis of Parkinson's disease.
MedLine Citation:
PMID:  20035637     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Parkinson's disease (PD) is a progressive neurological disorder marked by nigrostriatal dopaminergic degeneration and development of cytoplasmic aggregates known as Lewy bodies. The impact of this disease is indicated by the fact that mortality is two to five times as high among affected persons as among age-matched controls. However, the cause of PD is still unknown and no cure is available at present. Several biochemical abnormalities have been described in the brains of patients with PD, including oxidative stress and mitochondrial dysfunction. Recent identification of specific gene mutations that cause PD has further reinforced the relevance of oxidative stress and mitochondrial dysfunction in the familial and sporadic forms of the disease. The proteins that are reported to be related to familial PD-PTEN-induced putative kinase 1 (PINK1), DJ-1, alpha- synuclein, leucine-rich repeat kinase 2 (LRRK2), and, possibly, parkin-are either mitochondrial proteins or are associated with mitochondria, and all are involved in pathways that elicit oxidative stress or free radical damage. Mitochondria are continually exposed to reactive oxygen species and accumulate oxidative damage more rapidly than the rest of the cell. Therefore, Parkinson's disease has been suggested to be associated with mitochondrial dysfunction. Since mitochondria are the major intracellular organelles that regulate both cell survival and death, clarifying the involvement of mitochondrial dysfunction and biogenesis during the process of PD could provide treatment strategies that might successfully intervene in the pathogenesis and slow the progression of the disease.
Authors:
Tsu-Kung Lin; Cha-Wei Liou; Shang-Der Chen; Yao-Chung Chuang; Mao-Meng Tiao; Pei-Wen Wang; Jin-Bor Chen; Jiin-Haur Chuang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Chang Gung medical journal     Volume:  32     ISSN:  2309-835X     ISO Abbreviation:  Chang Gung Med J     Publication Date:    2009 Nov-Dec
Date Detail:
Created Date:  2009-12-28     Completed Date:  2010-03-10     Revised Date:  2013-10-22    
Medline Journal Info:
Nlm Unique ID:  101088034     Medline TA:  Chang Gung Med J     Country:  China (Republic : 1949- )    
Other Details:
Languages:  eng     Pagination:  589-99     Citation Subset:  IM    
Affiliation:
Department of Neurology, Chang Gung Memorial Hospital - Kaohsiung Medical Center, Chang Gung University College of Medicine, Niaosong Township, Kaohsiung County 833, Taiwan (R.O.C.).
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MeSH Terms
Descriptor/Qualifier:
Apoptosis
Biogenesis*
DNA, Mitochondrial / genetics
Dopamine / physiology
Humans
Mitochondria / physiology*
Oxidative Stress
Parkinson Disease / etiology*,  genetics
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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