Not Parkinsons, but we seem to be getting closer...
http://www.infobeat.com/stories/cgi/story.cgi?id=2556374906-bb9
New clue to nerve damaging diseases found-study
By Leslie Gevirtz
BOSTON (Reuters) - Medical researchers have uncovered a new
clue to help explain how some crippling diseases damage nerve
cells, a discovery that could lead to new treatments for
conditions like Huntington's chorea.
In separate papers appearing in Friday's issue of the
journal Cell, two research teams reported that such illnesses
seem to appear only when a key protein in a nerve cell slips
into the nucleus, the control center of the cell.
When the researchers used genetic engineering techniques to
prevent the accumulation of material in the nucleus, there were
no signs of Huntington's, which causes rapid, jerky movements
and relentless mental deterioration in 1 in 20,000 people.
The teams worked on inherited diseases caused by a
stuttering of the genetic code, where a section of the code is
repeated too many times. If there are more than 40 or so
repetitions, symptoms eventually appear.
But how the repeated sequences translate into an illness
remains a mystery.
Researchers, led by Harry Orr of the Institute of Human
Genetics at the University of Minnesota, discovered that if they
could prevent a protein known as ataxin-1 from entering the
nucleus, they could block the development of symptoms similar to
a group of human diseases known as spinocerebral ataxias.
The ataxias diseases affect about 1 in 50,000 people and
attack the same portion of the brain that causes intoxicated
persons to stagger. ``Some have to carry cards around saying
they are not intoxicated,'' and instead suffer from the
disorder, Orr said in a telephone interview.
The second study involved Huntington's chorea, a condition
characterized by a gradual decline and mental breakdown that
ends in insanity. Its first signs usually appear after the age
of 50.
Michael Greenberg of Children's Hospital in Boston and his
colleagues looked at how a different protein, spelled
huntingtin, caused the death of nerve cells growing in a test
tube. They found the cells died only when the nucleus was
invaded, this time by huntingtin.
The findings do not mean an imminent treatment for the
diseases. ``But we're really beginning to understand some
important aspects of the cell biology of this disease,'' said
Orr, whose genetic engineering techniques blocked the
development of ataxia in the mice.
``The next step is to try to do the same thing with a
drug,'' he said. ``We know how. We just need a specific agent.''
^REUTERS@
--
Judith Richards, London, Ontario, Canada
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