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Parkinson's disease mechanism discovered

Purdue performed the tests in rat neurons. Caldwell is also coordinator of HHMI's Undergraduate Research Intern Program at the University of Alabama.

"They all came back with the same answer," said Lindquist. "All saw significant suppression of toxicity; although none saw complete suppression, which confirms our yeast studies showing that other pathways are affected by alpha-synuclein accumulation. However, importantly, the results of our genetic screen have given us a way to ask important questions about these other aspects of alpha-synuclein toxicity," she said.

Lindquist also said the findings give important clues to why dopamine-producing neurons in the brain are the most vulnerable neurons to toxic alpha-synuclein accumulation. The death of such neurons reduces brain dopamine levels, causing the tremors and other symptoms of Parkinson's disease. Dopamine is one of many types of neurotransmitter -- chemical signals that one neuron launches at its neighbor to trigger a nerve impulse.

"Of all the neurotransmitters, dopamine has a higher potential for being toxic," she said. "Its toxicity is normally prevented in the neuron by sequestration within vesicles for transport from the ER. But a defect in ER trafficking caused by alpha-synuclein accumulation could cause the toxic buildup of dopamine to occur in these neurons."

Lindquist and her colleagues believe their findings will guide the search for new drugs that suppress alpha-synuclein toxicity by enhancing the machinery of ER-to-Golgi transport. Thus, she said, they have already conducted a screen of 150,000 compounds for those with therapeutic potential.

"We have found compounds that reverse alpha-synuclein toxicity, and we plan to publish those results soon," she said. "These findings are exciting because they tell us we have a platform for discovering new therapeutic strategies and for speeding the process of discovering treatments for these disorders."

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Source:Howard Hughes Medical Institute


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