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How Parkinson's Disease Protein Acts Like a Virus

A protein known to be a key player in the development of Parkinson's disease is able to enter and harm cells in the same way that viruses do, according to a Loyola University Chicago Stritch School of Medicine study.

The protein is called alpha-synuclein. The study shows how, once inside a neuron, alpha synuclein breaks out of lysosomes, the digestive compartments of the cell. This is similar to how a cold virus enters a cell during infection. The finding eventually could lead to the development of new therapies to delay the onset of Parkinson's disease or halt or slow its progression, researchers said.

The study by virologist Edward Campbell, PhD, and colleagues, was published April 25, 2013 in the journal PLOS ONE.

Alpha-synuclein plays a role in the normal functioning of healthy neurons. But in Parkinson's disease patients, the protein turns bad, aggregating into clumps that lead to the death of neurons in the area of the brain responsible for motor control. Previous studies have shown that these protein aggregates can enter and harm cells. Campbell and colleagues showed how alpha synuclein can bust out of lysosomes, small structures that collectively serve as the cell's digestive system. The rupture of these bubble-like structures, known as vesicles, releases enzymes that are toxic to the rest of the cell.

"The release of lysosomal enzymes is sensed as a 'danger signal' by cells, since similar ruptures are often induced by invading bacteria or viruses," said Chris Wiethoff, a collaborator on the study. "Lysosomes are often described as 'suicide bags' because when they are ruptured by viruses or bacteria, they induce oxidative stress that often leads to the death of the affected cell."
 
 

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