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RESEARCH ON PARKINSON’S and OXIDATIVE STRESS AT PUBMED
Gene. 2013 Aug 15. pii: S0378-1119(13)00993-1. doi: 10.1016/j.gene.2013.07.085. [Epub ahead of print]
The novel role of mitochondrial induced oxidative stress and genetic mutations in Parkinson’s disease.
Source: Molecular Physiology and Biophysics Laboratory, Department of Biological Sciences, Oakland University, Rochester, MI 48309
Abstract: Parkinson’s disease (PD) is recognized as one of the most advanced neurodegenerative diseases that produces pathogenic effects on an individual’s substantia nigra, a site of neurotransmitter dopamine. Memory and cognitive function are hindered by this disorder. It is understood that PD is age-related; as age increases, the chance of onset responds accordingly. Although genetic heritability influences the disease, the definite cause is unknown. A current hypothesis associates mitochondrial dysfunction, specifically reactive oxygen species (ROS), and oxidative stress (OS) as the fundamental agents of deterioration. Certain genetic mutations can also contribute to the mitochondrial misbalance producing OS. OS refers to the disequilibrium of free radicals and antioxidants saturated with ROS. Minor amounts of ROS are essential for normal physiological functions, playing a critical role in many biological processes. However, vast quantities of ROS production cause intracellular deregulation leading to continuous damage to critical cellular components such as membrane lipids, proteins, and DNA. This review expands on the specific impact of mitochondrial production of free radicals and its correlation to the neurodegeneration in Parkinson’s disease. http://www.ncbi.nlm.nih.gov/pubmed/23954870
Mitochondrial dysfunction is associated with neurodegeneration through many mechanisms. It can directly trigger cell death pathways that culminate in neuronal apoptosis or necrosis, disrupt calcium homestasis, and cause UPS dysfunction and oxidative stress. Dissecting the role of mitochondrial dysfunction in neurodegeneration is complicated by the fact that many of these downstream effects can themselves contribute to mitochondrial defects.
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