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Short idea (General)

Mitochondrial Biology in Parkinson's Disease
Yunjong Lee1,*
1Institute for cell engineering and Department of Physiology, Johns Hopkins University School of Medicine
*Corresponding author
  Received : June 02, 2009
  Accepted : June 03, 2009
  Published : June 05, 2009
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Synopsis

Parkinson's disease (PD) is a progressive neurodegenerative movement disorder. Identification of mutations in PD-associated genes has enabled focused study on cellular mechanisms of dopaminergic cell death as major feature of PD. Even though a lot of pathways have been mapped from the studies in vivo and in vitro, little effort has been directed at finding pathways which can be also applied to sporadic PD which, compared to other types of PD, dominates in PD patients. Since mitochondria have long been implicated as a major organelle contributing to specific dopaminerigc neuron degeneration in PD, in this review recent findings from PD research which are mainly related to mitochondrial pathology are addressed. Several PD genes are grouped in three distinct mitochondrial pathogenic pathways which include dysregulation of mitochondrial dynamics, production of reactive oxygen species (ROS) and impaired autophagy. PINK1/Parkin genetic interaction in mitochondrial fission is discussed with a brief touch on the underlying molecular mechanism. In addition, neuroprotective PD genes such as DJ-1, PINK1 and parkin are described in terms of their position in the defensive pathways against oxidative stress elicited by dysfunctional mitochondria. Finally, recent findings on parkin-mediated autophagic regulation of mitochondrial turnover are presented.

Keyword: Parkinson's disease, mitochondria, fusion/ fission, ROS, oxidative stress, autophagy, parkin, PINK1 and DJ-1
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