Followed Dale Severence's suggestion and took a little cyber trip to Emory's
website. I thought all of us may benefit from reading the material.
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RESEARCHERS USE NEW TECHNOLOGY TO LINK BRAIN CELL ENERGY DEFICITS TO
PARKINSON'S DISEASE

November 18, 1996
Media Contacts: Sarah Goodwin, 404/727-3366 - [log in to unmask]
Kathi Ovnic, 404/727-9371 - [log in to unmask]
http://www.emory.edu/WHSC/


WASHINGTON, D.C. -- Researchers at Emory University report at this week's
Society for Neuroscience meeting on the use of new technology to link brain
cell energy deficits to Parkinson's disease.

In the 1970s, some users of intravenous drugs suddenly developed severe,
permanent parkinsonism after injecting narcotics. Astute medical detective
work eventually found that the narcotics used by these drug users were
contaminated with a chemical called MPTP that killed the dopamine cells of the
brain. These are the same nerve cells that die in Parkinson's disease.

Laboratory research showed that MPTP killed the nerve cells by blocking the
cells' "power plants," called mitochondria. This finding then led researchers
to examine whether a similar problem with mitochondrial energy production
might cause Parkinson's disease, a debilitating illness that affects about one
million people in North America.

Several laboratories have found that the same mitochondrial energy deficits
caused by MPTP are found in the brains of patients who have died with
Parkinson's disease. It has been impossible, however, to determine whether
mitochondria in the brains of living Parkinson's patients are abnormal.

Emory University School of Medicine researchers have developed a new method to
examine mitochondria in the living brain using a technique called PET
(positron emission tomography) scanning. Shortly after intravenous injection
of a minute quantity of a radioactive "tracer," the tracer sticks to the
mitochondria and can be imaged with the PET scanner.

"Although only studies in animals have been performed so far, we expect to be
able to perform studies in Parkinson's patients soon," says Tim Greenamyre,
M.D., Ph.D., associate professor of Neurology at Emory. "This new technique
should also be useful for studying Alzheimer's disease, Huntington's disease,
stroke and epilepsy."

The question of why and how nerve cells die when they cannot produce enough
energy is also being examined. It turns out that when nerve cells cannot
produce sufficient energy they become susceptible to damage by one of the
brain's most abundant chemicals, glutamate.

Normally, glutamate is harmless and simply acts as a chemical messenger, or
neurotransmitter, for communication between nerve cells. However, when
mitochondria are not working properly, glutamate becomes a toxin that can kill
nerve cells. The researchers found that very mild mitochondrial damage
converts glutamate from a transmitter to a toxin.

Mitochondria normally produce their own toxic chemicals, known as "free
radicals." These free radicals usually cause little harm because mitochondria
also contain defense mechanisms against these toxins. One of the most
important is a chemical called glutathione, which detoxifies free radicals.
When mitochondria are damaged, as researchers believe is the case in
Parkinson's disease, they produce more free radicals. At the same time,
researchers have found that they make much less glutathione. In other words,
they make more toxin and have less ability to withstand it.

Besides functioning as cellular "power plants," mitochondria protect nerve
cells in other ways. One of the most important is protecting the cell from too
much calcium. The amount of calcium in a cell is normally controlled very
closely because excessive calcium can cause cell damage or death. When calcium
levels in a cell rise, mitochondria, in essence, vacuum up the calcium to
protect the cell. When mitochondria don't function optimally, calcium in a
cell can rise to abnormally high levels. Dr. Greenamyre and his Emory
colleagues are using a technique called laser scanning ell
mitochondria take up calcium and determine what happens when the mitochondria
malfunction.
They are also using this technique to study living cells from patients
known to have abnormal mitochondria.

"As we begin to understand how nerve cells die when their mitochondria
malfunction, we are exploring ways to protect the nerve cells," Dr. Greenamyre
says. "We have shown that drugs that block glutamate toxicity, glutamate
antagonists, are profoundly protective. This may provide a way to slow or stop
the normally progressive worsening of Parkinson's disease."

Amantadine, a drug used commonly to treat the symptoms of Parkinson's disease,
has been found to be a glutamate antagonist. A recent study found that the use
of amantadine was a predictor of improved survival in Parkinson's disease.
Similarly, drugs that prevent free radical damage are very protective against
mitochondrial damage, and there is great interest in testing their ability to
slow the progression of Parkinson's disease.


For more general information on The Robert W. Woodruff Health Sciences Center,
call Health Sciences News and Information at 404-727-5686, or send e-mail
to [log in to unmask]
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Parkinson's disease

Dr. Ray Watts is currently recruiting Parkinson's patients for a family
genetics study. Eligible
patients must have a family history of Parkinson's disease. For more
information, please call Celeste Duddleston, R.N., or Betty Wolthoff, R.N., at
404/72 7-8945.

Dr. Jorge Juncos is currently recruiting patients for two clinical drug trials
involving Parkinson's patients. Patients with early Parkinson's, preferably
untreated, are eligible for an MAOB inhibitor study. Parkinson's or
Parkinson's Plus patients with motor fluctuations are eligible for a glutamate
antagonist study. For more information, contact Colleen Wood, R.N., at
404/727-2629.

Drs. Jorge Juncos, Marian Evatt, and Rita Jewart are recruiting Parkinson's
patients who are experiencing hallucinations for a multicenter, open-label
study of the drug Seroquel. Patients who have not been treated with or who
have responded poorly to antipsychotic medications are eligible. For more
information, please call 404/728-6414.
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Margaret Tuchman(55yrs,dx1980) --NEW JERSEY
[log in to unmask]
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