The movie "Awakenings" shows the miraculous effects of the drug L-dopa. For 30 years, a brain infection caused the main patient character to languish in a coma, only to awake after a doctor gave him L-dopa.

For the half a million Americans with Parkinson's disease, L-dopa can be nearly as dramatic in relieving their physical symptoms -- the slow shuffling gait, the persistent trembling, the bouts of paralysis. These patients lack a key brain chemical, dopamine, which is replaced by the drug.

But as a treatment for Parkinson's, L-dopa is hardly miraculous. As the symptoms worsen, higher doses of the drug are needed. About four years after drug treatment begins, the increasing doses of L-dopa cause significant side effects in about half the patients, limiting its benefit.

That's why scientists have been searching for alternate drugs to slow the progression of symptoms and even prevent the disease from developing in the first place.

"We think people have the disease five, 10, 20 years before they get the symptoms," said J. William Langston, a neurologist who is president of the California Parkinson's Foundation. If patients could be identified early in their illness, he said, drugs now emerging from the laboratory may one day be able to slow or prevent it.

Last month, researchers at Schering AG, a pharmaceutical company in Berlin, reported in the British journal Nature that three new drugs were found in animal experiments to protect the brain from the effects of chemically induced Parkinson's disease. The new drugs clog proteins that open gateways into the nerve cells, preventing the Parkinson's-causing chemical from harming the nerve.

The next step is to test the drugs in human patients. While the animal tests are promising, scientists are cautious about the use of this type of drug in people because these drugs are known to cause memory loss. Already, researchers are looking for related compounds that have fewer side effects.

"All of a sudden, this field is moving forward," said Thomas Chase, chief of the National Institute of Neurological Disorders and Stroke's experimental therapeutics branch.

The first drug to emerge from this research explosion is deprenyl, now used as standard therapy for Parkinson's disease. Discovered 30 years ago, deprenyl prevents a normal brain enzyme from destroying dopamine and thus protects the dopamine-producing cells.

Last year, a large, federally financed study showed that deprenyl can slow to some extent the deterioration of people with Parkinson's. If doctors gave them the drug in the early stages of their disease, severe symptoms requiring L-dopa treatment were delayed an average of 18 months, compared to patients who did not get deprenyl. "Deprenyl is a major step forward," Chase said.

Another drug that works much like deprenyl but seems even more potent is now being tested in 200 patients in 14 research centers to see if it can be safely taken. The drug, made by Hoffmann-La Roche Inc., blocks the same enzyme as deprenyl. If results are encouraging, a Hoffman-La Roche spokesman said, the company will launch a larger trial to test the drug's effectiveness.

All of these drugs point to the strategy of early intervention to stop the disease before it develops into an incapacitating illness. The problem is identifying people who will succumb to Parkinson's.

"If we could find them, we could give them deprenyl {or some other drug} and perhaps prevent the disease from ever showing up," said Langston.

At this point, however, doctors can't predict who will get Parkinson's and would therefore benefit from preventive therapy. No blood test exists to identify people at high risk the way a cholesterol test identifies people at high risk of a heart attack. A Parkinson's diagnosis depends on a cluster of symptoms that show up after significant neurological damage already has occurred.

Last December, scientists on the Parkinson's Epidemiology Research Committee, a confederation of Parkinson's experts, reviewed several new developments that could lead to a quick diagnostic test.

William Parker Jr., a researcher at the University of Colorado Health Sciences Center in Denver, recently discovered that Parkinson's patients appear to have a defective enzyme in their platelets, the blood element involved in clotting. Other scientists have found the same defect in other tissues of the body, including the brain. If that enzyme turns out to be a marker for Parkinson's, a blood test could be developed to detect the disease.

Researchers also have found liver abnormalities in some patients with Parkinson's. The liver breaks down most of the toxic chemicals that enter the body. If a defect prevented the liver from destroying some chemical that kills brain cells, then the chemical could persist in the body long enough to cause Parkinson's disease. It might be possible to devise a blood test to measure such a defect in the liver.

Most people who develop Parkinson's are over age 60. The disease strikes men and women in equal numbers. There seems to be no inherited pattern to the disease.

Doctors believe that the loss of dopamine-producing cells is a normal part of aging as the brain loses thousands of nerve cells over a lifetime. But in patients with Parkinson's disease, the loss of dopamine-producing cells is much more pronounced, and symptoms arise when more than 80 percent of these nerve cells die.

Increasingly, researchers suspect that some chemical or chemicals in the environment -- natural or synthetic -- get into the body and accelerate the destruction of the dopamine-producing cells.

The environmental hypothesis received a boost in 1983 when some California drug addicts developed a severe form of Parkinson's after injecting a synthetic form of heroin. Parkinson Foundation's Langston, who was on the staff of the Santa Clara Valley Medical Center, where the addicts were treated, isolated the contaminant in the synthetic heroin. He discovered that the toxic contaminant destroyed the same dopamine-producing nerve cells in animals as the ones lost in patients with Parkinson's disease.

"That observation was revolutionary," said Caroline M. Tanner, a Parkinson's expert from Rush University in Chicago. It showed for the first time, she said, that a simple compound could get into the human brain and selectively destroy certain nerve cells. It also provided scientists with an animal model for designing better treatments.

While researchers do not believe the heroin contaminant is the cause of Parkinson's in older Americans, they suspect that related chemicals may be involved. Candidates include chemicals found in some pesticides and herbicides. Several studies suggest that living in rural areas, where the use of pesticides and herbicides is widespread, may increase a person's risk of developing Parkinson's.

William Koller, chairman of neurology at the University of Kansas Medical Center in Kansas City, in a study comparing 150 people with Parkinson's to a similar population of 150 people without the disease, found that those who developed the disease were two to three times more likely to have lived in a rural area and to have drunk well water than those who did not develop the disease.

"These studies are only suggestive," Koller cautioned. "There is something in the rural environment . . . but we don't know what {chemical} to point at."