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Advances in health and medicine.
Marjorie Bekaert Thomas
Advances in health and medicine.
Neurological Disorders Channel
Reported March 25, 2003

Potassium and Parkinson's

CHICAGO (Ivanhoe Newswire) -- Researchers from Northwestern University report symptoms of Parkinson's disease, a neurodegenerative disease afflicting over 1 million people in the United States, may be improved by blocking a specific potassium channel in a select group of brain cells.

The common symptoms of Parkinson's disease, including resting tremor, muscle rigidity and slowed movement, are the result of dopamine loss from the cell. Researchers have found a mechanism that may lessen the symptoms and slow progression of the disease.

Scientists say a potassium channel unique to the affected brain regions controls the cellular mechanism responsible for Parkinson's disease symptoms. The potassium channel, called Kv3.4, is found in a subset of neurons outside the basal ganglia. The basal ganglia are structures located deep in the brain that are responsible for normal movement such as walking. Neurons in another region of the brain contain high numbers of potassium channels that may account for the symptoms in Parkinson's disease patients.

Current therapies to surgically destroy these neurons or employ electrode stimulation to disrupt neuronal activity provide symptomatic relief. They also cause unwanted side effects such as uncontrolled movement. "The perfect therapy for Parkinson's disease would be to prevent neurons from exhibiting the behavior that causes the symptoms … without altering their 'good' behaviors," says researcher James Surmeier.

Blocking potassium channels with the Kv3.4 subunit or eliminating the subunit using gene therapy techniques are two possible therapeutic options, the authors write. Surmeier says, "Doing so would eliminate the 'bad' behavior but, importantly, preserve the 'good' behavior … of these neurons."

This article was reported by, who offers Medical Alerts by e-mail every day of the week. To subscribe, go to: /newsalert/.

SOURCE: Nature Neuroscience, 2003;6:258-266

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