Study - Parkinson's may affect nerves outside brain

WASHINGTON (Reuters) -- Parkinson's disease, caused by the loss of certain brain cells, may affect nerves throughout other organs of the body, researchers said Monday.

The discovery may affect the way the disease is treated and eventually lead to understanding what causes it, Dr. David Goldstein of the National Institute of Neurological Diseases and Stroke (NINDS) said.

Goldstein found that Parkinson's patients were lacking not only key brain cells, but also nerve endings in the heart.

"It's an enticing new idea, that whatever is causing the loss of sympathetic nerves in the heart is also causing the loss of dopamine-producing cells ... in the brain," Goldstein said in a telephone interview.

Parkinson's -- marked by episodes of freezing, lack of motor control, and eventual paralysis -- affects an estimated 500,000 to 1 million people in the United States, globally affecting about one out of every 100 people over the age of 65 and one in 50 over 80 years old.

There is no cure, and treatments only last a few years before they start adding to the debilitating symptoms. Well-known patients include actor Michael J. Fox and U.S. Attorney General Janet Reno.

What causes the symptoms is the loss of cells in a certain part of the brain that produce dopamine -- an important message-carrying chemical or neurotransmitter linked with movement.

But no one has been able to find out why those cells get destroyed in the first place.

Goldstein was not even looking for an answer to that question. He was studying patients with failure of the sympathetic nervous system, which affects blood pressure, pulse rate, perspiration, and other automatic responses to stress.

One key symptom is orthostatic hypotension -- a drop in blood pressure that comes when people stand up. Some patients have it all the time, complaining of dizziness and even fainting when they stand.

The symptom has been described in association with Parkinson's, and has sometimes been blamed on the drugs used to treat Parkinson's.

But Goldstein found this drop in blood pressure was associated with a loss of the sympathetic nerve endings. These nerve endings produce a neurotransmitter that is related to dopamine, called norepinephrine.

Writing in the Annals of Internal Medicine, Goldstein said he used positron emission tomography (PET) scans to detect the loss of these nerve endings in the heart.

It turned out that nearly all 29 Parkinson's patients in his study had this loss, even if they did not have the blood- pressure symptoms.

The discovery might open ways to find the underlying cause of Parkinson's, and might explain the unusual finding that heavy coffee drinkers seem to have a lower rate of Parkinson's, Goldstein said.

Norepinephrine and dopamine are both part of the same family of chemicals, called catecholamines -- as is a component of coffee called caffeic acid.

All three compounds -- dopamine, norepinephrine and caffeic acid -- are broken down in the body by an enzyme called COMT.

"Suppose somebody drank a lot of coffee. That person is taking in a lot of caffeic acid," Goldstein said, stressing that this theory is completely unsupported by any scientific studies.

"This cathecholamine could compete for COMT with ... dopamine and norepinephrine."

That would mean that, instead of getting rid of norepinephrine and dopamine, COMT could be tied up with the caffeic acid. This would make more of the two neurotransmitters available in the body and might explain why coffee could protect against Parkinson's, Goldstein said.

More research was needed, but the idea could open possibilities for treating Parkinson's, he said.

Copyright 2000 Reuters. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.

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National Parkinson Foundation, Inc.
The Parkinson's Network

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