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Scientists Find Toxin that Plays Key Role in Triggering Parkinson's Disease

by Thilaka Ravi on February 12, 2011 at 3:35 PM
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 Scientists Find Toxin that Plays Key Role in Triggering Parkinson's Disease

Scientists have identified a toxin produced by the brain that is responsible for the series of cellular events leading to Parkinson's disease.

After research in an animal model, investigators from Saint Louis University found that the brain toxin DOPAL plays a key role in killing the dopamine neurons which trigger the illness.

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Parkinson's disease is a debilitating neurodegenerative movement disorder, affecting 2 percent of individuals older than age 65 and 4 to 5 percent older than 85 years.

The disorder is due to a loss of dopamine neurons and is characterized by bradykinesia and tremors while at rest.

Dopamine, a vital chemical that allows for coordinated function of neurons controlling the body's muscles and movements, is produced by nerve cells in the substantia nigra.
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When 80 percent of these cells die or become damaged, symptoms of Parkinson's disease begin to appear, including tremors, slowness of movement, rigidity and stiffness, and difficulty with balance.

"In Parkinson disease, we knew that the death of dopamine cells is responsible for patients' symptoms. But no one knew why the cells are dying," said W. Michael Panneton, lead researcher.

From a cellular perspective, doctors know some pieces of the puzzle. They know that Parkinson patients have a loss of dopamine neurons in a part of the brain called the substantia nigra, leading to severe dopamine loss in another part of the brain called the striatum, and the aggregation of a protein called alpha-synuclein.

Alpha-synuclein is found throughout the brain. In some people, the protein clumps together. We found that it is DOPAL that causes alpha-synuclein protein in the brain to aggregate.

This induces further increases of DOPAL leading to the death of the dopamine-producing cells, which in turn causes Parkinson's symptoms to develop.

The study was published in PLoS One.

Source: ANI
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