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News in Brief

Study Suggests that Levodopa Does Not Hasten - and May Even Slow - Progression of PD
A study led by Columbia University scientists and published in the December 9 issue of The New England Journal of Medicine suggests that the commonly-used Parkinson's drug levodopa does not hasten the progression of Parkinson's disease - as some scientists had feared - and may actually slow it down.

Columbia University is a beneficiary of PDF's largest research grant.
The trial enrolled 361 early-stage Parkinson's patients and randomly divided them into four study groups. Three of the groups received levodopa in different doses and one received a placebo. After 40 weeks, the medication was withdrawn, and two weeks later, investigators used the Unified Parkinson's Disease Rating Scale (UPDRS) to assess disease progression. The results showed that participants from the levodopa groups experienced less decline overall than the placebo group, suggesting that levodopa does not speed disease progression and may even slow it.

"We still haven't found all of the answers we're looking for, but this is an important step in determining how levodopa affects Parkinson's disease progression. The results are encouraging, but we still have much more work to do before we can definitively explain the relationship between levodopa and Parkinson's progression," said Dr. Stanley Fahn, principal researcher of the study.

Researchers also performed brain scans on 142 patients at the beginning and end of the study to assess the presence of the dopamine transporter (an enzyme in the dopamine nerve terminals that serves as a biological marker of the progression of Parkinson's). These tests seemed to show that the levodopa patients had a greater loss of the dopamine transporter than placebo-treated patients, suggesting that levodopa may in fact speed up the loss of these brain cells. One explanation could be that levodopa, itself, inhibits the activity of the transporter.

The discrepancy between the results of the clinical examinations and the brain scans has led to debate among researchers. The central issue regarding the effect of levodopa on the long-term progression of Parkinson's remains unresolved by this study. No change in the way patients use levodopa is recommended at present. Investigators plan to continue their research into levodopa's role in the treatment of PD.

Alzheimer's Drug May Help People with Parkinson's
A report in the December 7 issue of The New England Journal of Medicine shows that Exelon® (rivastigmine tartrate), an Alzheimer's medication, may be moderately effective in the treatment of dementia in Parkinson's. This comes from the first large-scale, placebo-controlled clinical trial of a potential treatment for dementia in some PD patients.

Exelon, a dual cholinesterase inhibitor, is approved for treating Alzheimer's disease. The new report suggests that the product may also be useful in improving cognition and some aspects of behavior among people with Parkinson's disease.

The study enrolled 541 participants, who were randomly assigned to a placebo group or a treatment group taking increasing dosages of Exelon from 3 to 12 mg per day for 24 weeks. Using two Alzheimer's rating scales, investigators concluded that people in the Exelon treatment group experienced moderate improvements in cognitive symptoms (for example, memory impairments and attention problems) and behavioral problems such as agitation and mood swings, compared to participants taking placebo.

The most frequent side-effects reported with Exelon use were nausea, vomiting and a worsening of tremor.

The main limitation of the study is its short duration of only six months. Clinical experience with drugs for dementia often show declining benefits over time.

Gene Mutation Identified as Cause of Some Familial PD
In three separate studies, scientists have identified a new gene mutation in approximately five percent of cases of inherited Parkinson's disease, and in one-to-two percent of people who do not report a family history of the disease. This research, published in the January 18 online edition of The Lancet, is an important step forward in our understanding of the genetic component of Parkinson's.

Investigators from the National Institute on Aging (NIA) and scientists funded by the National Institute of Neurological Disorders and Stroke (NINDS) played important roles in this discovery, along with two international research teams. In two of the studies, Dr. Vincenzo Bonifati of Erasmus Medical Centre, the Netherlands, and Dr. William Nichols of Cincinnati Children's Hospital Medical Center independently analyzed people who reported a high incidence of Parkinson's in their families. The two groups used the data to confirm that a single mutation on the recently discovered LRRK2 gene causes Parkinson's in five percent of people with a family history of PD.

A third study, led by Dr. Nicholas Wood of the National Hospital for Neurology and Neurosurgery in London, analyzed Parkinson's patients who do not have a family history of the disease. His team determined that the mutation also causes one-to-two percent of Parkin-son's disease in people without inherited PD.

Dr. Juliette Harris, Genetic Counselor at Columbia University Medical Center, emphasizes that while this is an important and exciting discovery, it still does not account for the cause of PD in the majority of people.

"It is now becoming increasingly clear that Parkinson's is caused by numerous genetic factors and environmental factors," she told PDF News & Review. "It is therefore even more crucial that research focus on identifying these risk factors and use this knowledge to fight Parkinson's disease."

Research Points to Link Between Exercise and Parkinson's
Data from a study published in the February 22 edition of Neurology indicate that men who exercise regularly and strenuously in early adult life may have a lower risk of dev-eloping Parkinson's disease in later years, as compared to men who did not exercise. The study, conducted by Dr. Alberto Ascherio and colleagues at the Harvard School of Public Health, suggests that for men, exercise is neuroprotective. The study did not establish a possible link for women between exercise and the risk of Parkinson's.

Researchers examined information collected from two large studies, the Health Professionals Follow-Up Study and the Nurses' Health Study. Participants completed questionnaires on lifestyle, disease history and physical activity beginning in 1986 and then updated the information every two years through 2000. The respondents (48,574 men and 77,254 women) were all middle-aged or older at the start of the survey. A total of 387 of them (252 men and 135 women) had been diagnosed with Parkinson's during the course of the study.

The scientists found that as male physical activity increased, the risk of Parkinson's disease seemed to decrease. Men who were the most physically active at the start of the study cut their risk of developing Parkinson's disease by 50 percent compared to men who were the least physically active. Although the data did not reveal the same relationship between Parkinson's and exercise for women, researchers point out that much or all of the difference might be explained by the fact that the women surveyed grew up during a time when there was less emphasis on exercise for females.

These results seem to coincide with the findings of some animal studies, such as the work of Dr. Michael Zigmond and his colleagues at the University of Pittsburgh. In Dr. Zigmond's work, rats were forced to exercise for seven days before being treated with chemicals to induce Parkinson's disease. The rats that had exercised showed significantly less cell death of dopamine-containing neurons than sedentary rats. Based on this information, Dr. Zigmond's group has begun a small pilot study in Parkinson's patients to learn more about the possible relationship between exercise and PD in humans.