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Yusuf Hamied Department of Chemistry

 

Image courtesy Alfonso De Simone

Department of Chemistry researchers and their collaborators have identified important clues about what may be happening to patients when a protein associated with Parkinson's Disease malfunctions.

Researchers have established how a protein called alpha-synuclein, which is closely associated with Parkinson’s Disease, functions in healthy human brains. By showing how the protein works in healthy patients, the study offers important clues about what may be happening when people develop the disease itself.


Parkinson’s Disease is one of a group of conditions known as “protein misfolding diseases”, because they are characterised by specific proteins becoming distorted and malfunctioning. These proteins then cluster into thread-like chains, which are toxic to other cells.


While malfunctioning alpha-synuclein has long been recognised as a hallmark of Parkinson’s Disease, its role in healthy brains was not properly understood until now. The new study, carried out by researchers in this department and Imperial College London, shows that the protein regulates the flow of cellular transporters known as synaptic vesicles – a process fundamental to effective signalling in the brain.


Significantly, the researchers also tested mutated forms of alpha-synuclein that are linked to Parkinson’s disease. This was found to interfere with the same mechanism, essentially by impairing the ability of alpha-synuclein to regulate the flow of synaptic vesicles, and hence compromising the signalling between neurons.


Giuliana Fusco, a Chemistry PhD student, carried out the main experiments underpinning the research. “It was already clear that alpha-synuclein plays some sort of role in regulating the flow of synaptic vesicles at the synapse, but our study presents the mechanism, explaining exactly how it does it,” she said. “Because we have shown that mutated forms of alpha-synuclein, which are associated with early onset familial forms of Parkinson’s Disease, affect this process, we also now know that this is a function that may be impaired in people who carry these mutations.”


The researchers stress that the results should be treated with caution at this stage, not least because much about Parkinson’s Disease remains obscure.


This article has been taken with permission from a longer version on the University of Cambridge research web pages.