To : List Members
 
 From: Joe Imperiale
           [log in to unmask]
 
     I recently read an article on the recent discovery of a PD gene.  I
wrote to AOL and requested their permission to distribute the article out on t
he PD information exchange network.  The permission to distribute and the
article follows:
 
Subj:   Re:FINDING AOL SERVICES
Date:   95-04-11 18:26:45 EDT
From:   [log in to unmask]
 
From: [log in to unmask] (Technical Support)
To: [log in to unmask]
 
Dear HJPJA,
 
I am writing on behalf of America Online to respond to your recent E-mail.
 
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--------------------
 
Original Letter:
Hi, my name is Joe Imperiale. I belong to the Parkinson Disease
Information Exchange Network. I recently read an article on the discovery of
a Parkinsons Disease gene on AOL. I want to put it out on the exchange but I
thought I should ask permission first, and I thought this would be a good
place to start.
    I am looking forward to hearing from you soon. Please let me know if you
want me to transmit the entire text to you so you can read it if you need to.
 
                                  Best Regards
                                   Joseph M. Imperiale  [log in to unmask]
 
 
 
 
 
--------------------
 
 
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Subject: Re:FINDING AOL SERVICES
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***********************************************************************
 
The article on the discovery of a PD gene follows:
 
PARKINSON'S DISEASE GENE DISCOVERED
 
     ST.LOUIS- The discovery of a gene associated with a rare
form of Parkinson's disease provides researchers with a long
sought piece to the puzzling pathogenesis of this disease.
 
     A team of researchers at Washington University School of
Medicine in St. Louis have characterized a rare disease,
aceruloplasminemia, that causes a rare form of Parkinson's.
Aceruloplasminemia is caused by a mutation in the ceruloplasmin
gene, which is involved in iron transport.
 
     Patients with this gene mutation do not make ceruloplasmin,
a protein that removes iron from cells. The iron then accumulates
in cells in the brain's basal ganglia region and causes
neurological problems. These include  the tremors and gait
abnormalities
associated with Parkinson's disease, according to Jonathan D.
Gitlin, M.D., associate professor of pediatrics, Washington
University School of Medicine.
 
     Neurologists have long hypothesized that Parkinson's disease
results from a combination of genetic and environmental factors.
The current  discovery is important because it is the first time
a genetic cause of Parkinson's disease has been identified.
 
     "This is a clearly defined piece of the puzzle and there
haven't been many of those in this particular disease. I think
that's what's most exciting," Gitlin said.
 
     Gitlin and colleagues discovered the genetic form of
Parkinson's during a study of a Japanese family that had
Parkinson symptoms and low levels of ceruloplasmin. Autopsy and
biopsy analyses of brain and liver tissue of a different Japanese
patient  led to the conclusion that this abnormality was caused
by increased iron deposition. Gitlin's lab then obtained DNA from
another Japanese family and identified a mutation on the
ceruloplasmin
gene located on chromosome 3. All of the patients with the
mutation
had basal ganglion damage characteristic of Parkinson's disease
 
 
     This finding gives researchers important new information
which could lead to innovations in the diagnosis and treatment of
 Parkinson's disease. Genetic screening based on these findings
may also help doctors diagnose patients with neurologic disorders
for which no cause is known. Ultimately, the identification of
this
mutation could help prevent the onset of Parkinson's disease.
 
  "Hopefully, if you find out early, it might be the kind of
disease that if there was some kind of therapy, you could prevent
it," he said.
 
     Dr. Gitlin believes this form of Parkinson's disease has
been underdiagnosed in the past. He recommends that patients with
undiagnosed movement disorders ask their doctors to look for
aceruloplasminemia.
 
     Scientists have known for some time what neurotransmitter is
depleted in Parkinson's disease patients (dopamine) and where it
is depleted (the basal ganglia). What is not known is what
initiates and maintains this neurodegenerative process. Some
studies have hinted at familial linkages while others have
implicated environmental factors ranging from drinking water and
cycad nuts to toxic drugs and poor education.
 
    Earlier this year Swedish researchers reported data from
animal studies supporting the hypothesis that Parkinson's is
caused by a lack of sufficient dopaminotrophic support.
Researchers at the Karolinska institute in Stockholm conducted a
series of experiments in mice using a cloned version of a natural
 protein associated with nerve cell growth called glial cell
line-derived
neurotrophic factor (GDNF).
 
     The researchers concluded that intracerebral GDNF
administration exerts both protective and reparative effects on
the nigrostriatal dopamine system, which may have implications
for the development of new treatment strategies for Parkinson's
disease.
 
     Dr. Gitlin's research appears in the March 28 issue of the
Proceedings of the National Academy of Sciences. The Swedish data
appeared in Nature, Olson et al., v.373, 1/26/95.
 
BACKGROUND
 
     Nearly one million people in the U.S. have Parkinson's
disease. This is a mysterious disease with no known cause or
cure. The cause of Parkinson's disease is currently thought to be
a combination of environmental and genetic factors.
 
     The symptoms of Parkinson's disease were first described by
British physician Dr. James Parkinson in 1812. The first symptom
is often an involuntary tremor. As the disease progresses, the
muscles become stiff and the face loses all expression. Patients
also develop difficulty walking and standing.
 
     The first treatment breakthrough came with levadopa. The
drug essentially replaces the lost dopamine in the brain.
However, large doses are required, resulting in undesirable side
effects, such as nausea, heart problems & dementia. The
subsequent development of carbidopa, which is given in
conjunction with levadopa, allows a smaller dose of levadopa to
be used, resulting in fewer side effects.
 
     Many patients respond well at first to this combination
therapy, but after a couple years of treatment the effects may
begin to wear off. At the same time, prolonged use of levadopa
can have serious side effects including involuntary movements of
the limbs and psychological disturbances.
 
       A new treatment called seligiline has recently become
available which has a completely different mechanism of action
from levadopa. The drug is potent inhibitor of an enzyme called
'monoamine oxidase B' which breaks down dopamine. This means more
dopamine can be preserved in the brain. The drug appears to have
a neuroprotective effect and may delay the onset of Parkinson's
symptoms.
 
                         ***
 
 
 
Transmitted:  95-03-29 19:26:06 EST
 
 
                                  Best Regards To All
                                  Joseph M. Imperiale
                                  [log in to unmask]