Washington: Overexpression of a protein can disrupt vital recycling processes in neurons leading to development of Parkinson`s disease – a neurodegenerative movement disorder.
Researchers at the University of California, San Diego School of Medicine found that overexpression of the alpha-synuclein protein appears to disrupt vital recycling processes in neurons.
It starts with the terminal extensions of neurons, working its way back to the cells` center, with the potential consequence of progressive degeneration and eventual cell death.
"This is an important new insight. I don`t think anybody realised just how big a role alpha-synuclein played in managing the retrieval of worn-out proteins from synapses and the role of alterations in this process in development of PD," said principal investigator Mark H Ellisman.
Parkinson`s disease is characterised by the gradual destruction of select brain cells that produce dopamine, a neurotransmitter involved in regulating movement and emotion.
Researchers, with colleagues at the University of Illinois, Urbana, focused upon one of those gene products: alpha-synuclein.
They found that excess levels of alpha-synuclein accumulated in the presynaptic terminal - part of the junction where axons and dendrites of brain cells meet to exchange chemical signals.
"The over-expression of alpha-synuclein caused hypertrophy in these terminals. The terminals were enlarged, filled with structures we normally don`t see," said Daniela Boassa, the study`s first author.
Boassa said that as alpha-synuclein accumulates in the terminals, it appears to hinder normal degradation and recycling processes in neurons. This would progressively impair the release of neurotransmitters. In time, the neurons might simply stop functioning and die.
"Other studies have noted that PD is characterised by progressive loss of vesicle traffic, and neurotransmitter release. Our study provides a structural and mechanistic explanation for why that happens," Boassa said.
The study was published in The Journal of Neuroscience.