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Nerve cell protein may shed light on Parkinson's

  [ 6 votes ]   [ Discuss This Article ] • August 8, 2000

Scientists have found that a protein called synuclein, which is found in nerve cells, plays a role in the communication between neurons. This may provide an important clue to the mechanisms underlying some types of Parkinson's and other devastating neurological diseases.

Since 1997, the nervous system protein known as alpha-synuclein has been implicated in mechanisms leading to the cause and progression of Parkinson's disease.

Apha-synuclein filaments form a dense meshwork within neurons that could deprive the cells of essential proteins and lead to degeneration, a hallmark of several neuro-degenerative disorders, including Alzheimer's disease.

"Clarifying what happens in Parkinson's will have a profound impact on understanding mechanisms underlying all of these disorders and on efforts to develop more effective therapies to treat them," says the study's lead author, Virginia Lee, Ph.D., a neurobiologist at the University of Pennsylvania in Philadelphia. The study, funded by the Alzheimer's Association and the National Institutes of Health, appears in the May 1 issue of The Journal of Neuroscience.

Parkinson's afflicts an estimated 500,000 Americans; Alzheimer's, roughly 4 million.

In the study, Lee and her colleagues examined the normal function of synucleins using cultures of neurons from the hippocampus, a banana-shaped brain structure known to be important for learning and memory. They found that by reducing the expression of synucleins, the number of cell structures capable of communicating between neurons was greatly reduced.

"Virginia Lee and her colleagues have provided strong evidence that synucleins control the release of neurotransmitters from nerve cells," says Paul Greengard, Ph.D., who studies these proteins at Rockefeller University in New York. "This is a very important discovery about a family of proteins which have been implicated in both Parkinson's disease and in Alzheimer's disease."

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