A small protein previously associated with cell dysfunction and death plays a critical role in repairing breaks in DNA, according to new research led by scientists at Oregon Health & Science University. The results were published in Scientific Reports.
This research represents the first demonstration of the role that alpha-synuclein 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.
Aggregates of alpha-synuclein, known as Lewy bodies, have long been implicated in Parkinson's and other forms of dementia but this new study casts a new light on that process. Lewy bodies seem to be problematic because they pull alpha-synuclein protein out of the nucleus of brain cells. The current research reveals that these proteins perform a crucial function by repairing breaks that occur along the vast strands of DNA present in the nucleus of every cell of the body.
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.
“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.”
Unni 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.
