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      Role of Oxidative Stress in Parkinson's Disease

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          Abstract

          Parkinson's disease (PD) is a progressive neurodegenerative movement disorder associated with a selective loss of the dopamine(DA)rgic neurons in the substantia nigra pars compacta and the degeneration of projecting nerve fibers in the striatum. Because there is currently no therapy that delays the neurodegenerative process, modification of the disease course by neuroprotective therapy is an important unmet clinical need. Toward this end, understanding cellular mechanisms that render the nigral neurons particularly vulnerable have been a subject of intensive research. Increasing evidence suggests that oxidative stress plays a major role. The metabolism of DA itself contributes to oxidative stress, resulting in modification of intracellular macromolecules whose functions are important for cell survival. Mitochondrial dysfunction and the consequent increase in reactive oxygen species also trigger a sequence of events that leads to cell demise. In addition, activated microglia produce nitric oxide and superoxide during neuroinflammatory responses, and this is aggravated by the molecules released by damaged DAergic neurons such as α-synuclein, neuromelanin and matrix metalloproteinase-3. Ways to reduce oxidative stress therefore can provide a therapeutic strategy. NAD(P)H:quinone reductase (NQO1) and other antioxidant enzymes, whose gene expression are commonly under the regulation of the transcription factor Nrf2, can serve as target proteins utilized toward development of disease-modifying therapy for PD.

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          Author and article information

          Journal
          Exp Neurobiol
          Exp Neurobiol
          EN
          Experimental Neurobiology
          The Korean Society for Brain and Neural Science
          1226-2560
          2093-8144
          March 2013
          31 March 2013
          : 22
          : 1
          : 11-17
          Affiliations
          Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138-736, Korea.
          Author notes
          To whom correspondence should be addressed. TEL: 82-2-3010-4279, FAX: 82-2-3010-4248, oyhwang@ 123456amc.seoul.kr
          Article
          10.5607/en.2013.22.1.11
          3620453
          23585717
          Copyright © Experimental Neurobiology 2013.

          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.

          Categories
          Review Article

          Neurosciences

          parkinson's disease, dopamine, oxidative stress, neuroinflammation, mmp-3, nqo1

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