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Improper protein digestion in neurons identified as a cause of familial Parkinson's
Date:3/5/2013

NEW YORK, NY (March 5, 2013) Researchers at Columbia University Medical Center (CUMC), with collaborators at the Albert Einstein College of Medicine of Yeshiva University, have discovered how the most common genetic mutations in familial Parkinson's disease damage brain cells. The mutations block an intracellular system that normally prevents a protein called alpha-synuclein from reaching toxic levels in dopamine-producing neurons. The findings suggest that interventions aimed at enhancing this digestive system, or preventing its disruption, may prove valuable in the prevention or treatment of Parkinson's. The study was published March 3 in the online edition of the journal Nature Neuroscience.

Parkinson's disease is characterized by the formation of Lewy bodies (which are largely composed of alpha-synuclein) in dopamine neurons. In 1997, scientists discovered that a mutation in alpha-synuclein can lead to Lewy body formation. "But alpha-synuclein mutations occur in only a tiny percentage of Parkinson's patients," said co-lead author David L. Sulzer, PhD, professor of neurology, pharmacology, and psychiatry at CUMC. "This meant that there must be something else that interfered with alpha-synuclein in people with Parkinson's."

Dr. Sulzer and his colleagues suspected that a gene called leucine-rich repeat kinase-2 (LRRK2) might be involved. LRRK2 mutations are the most common mutations to have been linked to Parkinson's. The current study aimed to determine how these mutations might lead to the accumulation of alpha-synuclein.

"We found that abnormal forms of LRRK2 protein disrupt a critical protein-degradation process in cells called chaperone-mediated autophagy," said Dr. Sulzer. "One of the proteins affected by this disruption is alpha-synuclein. As this protein starts to accumulate, it becomes toxic to neurons." Delving deeper, the researchers found that LRRK2 mutations interfere with LAMP-2A, a lysosome membrane receptor
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Contact: Karin Eskenazi
ket2116@columbia.edu
212-342-0508
Columbia University Medical Center
Source:Eurekalert

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