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According to a new study by scientists at Oregon Health & Science University, a small protein previously badociated with cell dysfunction and death actually plays a vital role in repairing DNA breaks.
The discovery, published today in the journal Scientific reports, marks the first demonstration of the role that alpha-synuclein plays in preventing the death of neurons in brain diseases such as Parkinson's disease, 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 or stimulate the function of alpha-synuclein in people with Parkinson's disease and other neurodegenerative disorders.
Aggregates of alpha-synuclein, known as Lewy bodies, have long been badociated with Parkinson's disease and other forms of dementia.
The study released today sheds new light on this process.
The results suggest that Lewy bodies are problematic because they extract alpha-synuclein protein from the nucleus of brain cells. The study, which examined live mouse cells and post-mortem brain tissue in humans, revealed that these proteins perform a crucial function in repairing breakages that occur along the vast strands of hair. DNA present in the nucleus of each cell of the body.
The role of alpha-synuclein in DNA repair can be crucial in preventing cell death. This function can be lost in brain diseases such as Parkinson's disease, leading to the widespread death of neurons.
"It may be the loss of this function that kills this cell," said lead author Vivek Unni, M.D., Ph.D., an badociate professor of neurology at the OHSU School of Medicine.
The researchers found that alpha-synuclein protein was rapidly recruited to the site of DNA damage in mouse neurons. In addition, they found an increase in the number of double-strand breaks in the DNA of human and mouse tissues in which the protein was pooled as Lewy bodies in the cytoplasm surrounding the nucleus of the cell. Taken together, the results suggest that alpha-synuclein plays a crucial role in binding broken strands of DNA to the nucleus of the cell.
In other words: if alpha-synuclein are factory workers, it's as if all gathered for an extended coffee break and left the machines unattended.
Unni, who is also seeing patients under the OHSU Parkinson Center and Movement Disorders program, said he hoped these findings would lead to the development of methods to introduce alpha-synuclein proteins into the system. the nucleus of cells or devise methods to replace its functions.
"It's the first time anyone finds out that one of its functions is DNA repair," Unni said. "It's essential for cell survival and it seems like it's a lost function in Parkinson's disease."
The work of this study was funded in part by National Institutes of Health grants NS102227, NS096190, NS069625, NS061800, AG024978, AG008017 and T32AG055378. a postgraduate research grant from the National Science Foundation, the Kinnie Family Foundation, the Oregon Partnership for Alzheimer's Research and the American Parkinson Disease Association.
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Material provided by University of Health and Sciences of Oregon. Note: Content can be changed for style and length.
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