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)
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