For the last several years, neurologists have been probing a connection between Parkinson's disease and problems with mitochondria, the miniature power plants of the cell.
Toxins that mimic Parkinson's effects act specifically to poison mitochondria, and mitochondria appear to be damaged in the brain cells that are endangered in the disease. But one unresolved question has been: are mitochondria simply the vulnerable "canaries in the coal mine" or is their deterioration a key step on the way to neurodegeneration? Now researchers at Emory University School of Medicine have found that a protein called MEF2D, which helps brain cells withstand stress and toxins, also plays an unexpected role inside mitochondria. MEF2D's ability to keep mitochondria well tuned appears to be especially sensitive to impairment in Parkinson's disease, the research team found. The results will be published online in the Journal of Clinical Investigation. "Our data suggest that problems with MEF2D in mitochondria could represent one of the earlier steps in the progress of the disease," says senior author Zixu Mao, PhD, associate professor of pharmacology and neurology at Emory University School of Medicine. Postdoctoral researcher Hua She, PhD, was the first author. The Emory team showed that MEF2D binds one particular mitochondrial gene, ND6, which is necessary for assembly of complex I. Complex I begins the electron transport process that is necessary for mitochondria to function. Mitochondria are thought to have evolved from bacteria that once lived independently, but were engulfed and harnessed by a primitive cell millions of years ago. Mao and his colleagues found an example of how this symbiosis has extended to having proteins like MEF2D turn on genes inside mitochondria.Source:MedIndia
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