Cellular damage induced by oxygen free radicals may be one important factor contributing to Parkinson’s disease, reports a new study. //This groundbreaking study conducted by neuroscientists at the University of Virginia Health System highlights that damage of complex I, a protein that plays a major role in the electron transport chain inside the mitochondria has been blamed for cellular damage in Parkinson’s disease.
Using the brain cells from deceased Parkinson’s patients who donated to the UVa brain bank, Dr. Jim Bennett, a UVa neurologist, and colleagues, isolated complex I from the mitochondria of ten Parkinson’s brains and compared them to the complex I proteins from twelve normal brains. They discovered that the complex I assembly in Parkinson’s had 50 percent more damage from oxygen. The complex I in Parkinson’s brains also had evidence of not being properly assembled and had reduced electron flow, Bennett said.
‘This part of the protein complex is being damaged by oxygen free radicals more in a brain with Parkinson’s than it is in someone of same age who does not have PD,’ Bennett said. His research is published in the May 10th edition of the Journal of Neuroscience.
Oxygen free radicals are oxygen molecules that carry an extra electron. They are destructive because, in excessive amounts, they chemically attack the components of the cell, including proteins, DNA and lipids in cell membranes. One of the major problems of normal aging is an increased level of these free radical damaged proteins, along with damaged DNA and lipids.
Bennett believes that Parkinson’s patients may benefit one day from drugs that can slow the damage from free radicals. ‘If we could soak up the free radicals in mitochondria, then complex I could repair itself,’ Bennett said. ‘If this damage is caught in people early on, we might interrupt the progression of Parkinson’s disease. Such treatment is hypothetical at this point, but it is rational.’
Right now, Bennett and his colleagues don’t know why complex I was damaged in the Parkinson’s patients. ‘It could be that something has gone terribly wrong with the mitrochondrial genome passed down by a person’s mother that codes for several proteins in complex I,’ Bennett said. ‘Something could be wrong in the coding for genes that help complex I assemble. Or there could be environmental toxins. Our research is a first real step in understanding at a detailed biochemical level what the challenge is.’
Bennett said he now plans to model the observation by extracting mitochondrial DNA from the cells of donated PD brains, put the DNA into a cell and express it to see if the phenomenon can be eproduced.
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