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ID 115630
Author
Ogino, Mako Nara Women's University
Nakano, Noriko Nara Women's University
Minami, Akari Nara Women's University
Kitagishi, Yasuko Nara Women's University
Matsuda, Satoru Nara Women's University
Keywords
oxidative stress
ROS
DNA repair
PTEN
BRCA1
estrogen
Parkinson’s disease
Content Type
Journal Article
Description
Oxidative stress is considered to play key roles in aging and pathogenesis of many neurodegenerative diseases such as Parkinson’s disease, which could bring DNA damage by cells. The DNA damage may lead to the cell apoptosis, which could contribute to the degeneration of neuronal tissues. Recent evidence suggests that PTEN (phosphatase and tensin homolog on chromosome 10) may be involved in the pathophysiology of the neurodegenerative disorders. Since PTEN expression appears to be one dominant determinant of the neuronal cell death, PTEN should be a potential molecular target of novel therapeutic strategies against Parkinson’s disease. In addition, defects in DNA damage response and DNA repair are often associated with modulation of hormone signaling pathways. Especially, many observations imply a role for estrogen in a regulation of the DNA repair action. In the present review, we have attempted to summarize the function of DNA repair molecules at a viewpoint of the PTEN signaling pathway and the hormone related functional modulation of cells, providing a broad interpretation on the molecular mechanisms for treatment of Parkinson’s disease. Particular attention will be paid to the mechanisms proposed to explain the health effects of food ingredients against Parkinson’s disease related to reduce oxidative stress for an efficient therapeutic intervention.
Journal Title
International Journal of Molecular Sciences
ISSN
14220067
16616596
NCID
AA12038549
Publisher
MDPI
Volume
17
Issue
6
Start Page
954
Published Date
2016-06-15
Rights
© 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).
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DOI (Published Version)
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language
eng
TextVersion
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departments
Medical Sciences