U.S. study paves way for new treatments for Parkinson's, other brain diseases
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E-mail Xinhua, July 31, 2019
LOS ANGELES, July 30 (Xinhua) -- A small protein previously associated with cell dysfunction and death serves a critical function in repairing breaks in DNA, according to new research led by scientists at Oregon Health and Science University (OHSU).
The discovery, published Monday in the journal Scientific Reports, marked the first demonstration of the role that alpha-synuclein protein plays in preventing the death of neurons in brain diseases such as Parkinson's, which affects 1.5 million people in the United States alone.
The findings suggest that it may be possible to design new therapies to replace alpha-synuclein's function or boost it in people with Parkinson's disease and other neurodegenerative disorders, according to the study.
Aggregates of alpha-synuclein, known as Lewy bodies, have long been connected to Parkinson's and other forms of dementia. The study casts a new light on that process.
Alpha-synuclein's role in DNA repair may be crucial in preventing cell death. This function may be lost in brain diseases such as Parkinson's, leading to the widespread death of neurons.
Researchers found that the alpha-synuclein protein rapidly recruited to the site of DNA damage in the neurons of mice. In addition, they found increased double-strand breaks in the DNA of human tissue and mice in which the protein was clumped together in the form of Lewy bodies in the cytoplasm surrounding the cell's nucleus. The results suggest that alpha-synuclein plays a crucial role in binding broken strands of DNA within the cell's nucleus.
Vivek Unni, an associate professor of neurology in the OHSU School of Medicine, said he hopes that these findings lead to the development of methods to deliver alpha-synuclein proteins into the nucleus of cells or designing methods to replace its function.
"This is the first time that anyone has discovered one of its functions is DNA repair," Unni said. "That's critical for cell survival, and it appears to be a function that's lost in Parkinson's disease." Enditem
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