Could someone interpret/translate? =20 =20 Cellular Defect In Parkinson's Disease Linked To Mitochondrial Mutatio= n WESTPORT, Oct 11 (Reuters) - Investigators have tracked a defective=20 cellular mechanism associated with Parkinson's disease to a genetic defec= t=20 in mitochondria, and shown that it "...may play an important role in the= =20 neurodegeneration of [Parkinson's disease]. Dr. W. Davis Parker of the University of Virginia, Charlottesville,=20 explains in the October Annals of Neurology that the mitochondrial electr= on=20 transport enzyme NADH:ubiquinone oxidoreductase, known as complex I, is=20 defective in multiple tissues in persons with Parkinson's disease. However, complex I is encoded by both mitochondrial DNA and nuclear=20 DNA, and "...the origin of this lesion and its role in the neurodegenerat= ion=20 of PD are unknown." Dr. Parker and colleagues now show that the complex I defect stems f= rom=20 mitochondrial DNA and interferes with the function of mitochondria. They=20 developed a cell line lacking mitochondrial DNA, and inserted mitochondri= a=20 from Parkinson's disease patients or control subjects. The parkinsonian =20 cells showed, "... a stable 20% decrement in complex I activity [and]=20 increased oxygen radical production," as well as increased susceptibility= to=20 the parkinsonism-inducing toxin, MPTP. The investigators conclude that the complex I defect is genetic, and= =20 that it fosters reactive oxygen species which might confer increased=20 neuronal susceptibility to toxins. In a University of Virginia press release, study co-author Dr. Russe= ll=20 Swerdlow comments that "While the genetically determined complex I defect= in=20 Parkinson's disease may itself be sufficient to produce the disease, our=20 research does not rule out the importance of external toxins in the disea= se=20 process. The observation that a specific biochemical defect can render ce= lls more vulnerable to MPTP toxicity illustrates how interactions between an=20 environmental mitochondrial toxin and an apparent mtDNA defect could=20 accelerate neurodegeneration. This may explain why some individuals devel= op=20 Parkinson's disease following toxin exposure, while others similarly=20 subjected to the same toxin at the same dose do not." Ann Neuro 1996:40;663-671. -Westport Newsroom 203 221 7648 Copyright =A9 1996 Reuters Limited. Margaret Tuchman(54yrs,dx1980) [log in to unmask] ******************************************************************* Satisfaction Guaranteed or your Smile cheerfully Refunded