Mouse model confirms mutated protein plays role in dementia

LONDON - A new mouse model that confirms that mutations of a protein called beta-synuclein promote neurodegeneration has been created by a team of scientists from Japan and the University of California, San Diego School of Medicine.

The discovery creates a potential new target for developing treatments of diseases like Parkinson’s and Alzheimer’s.

The newly published research describes the creation of a transgenic mouse model that expresses the B-synuclein mutation. The mice suffer from neurodegenerative disease, validating La Spada’s earlier work.

“Beta-synuclein is interesting because it is closely related to alpha-synuclein, a protein that can cause Parkinson’s disease by being mutated or over-expressed,” La Spada said.

“A-synuclein is viewed as central to Parkinson’s disease pathogenesis. The question has been: could B-synuclein also promote neurodegeneration because it’s similar in its sequence and expression pattern to A-synuclein? This study shows that the answer is yes.”

These findings, said La Spada, establish B-synuclein’s links to Parkinson’s disease and related disorders, making it a new and, now, proven target for potential therapies.

The work has been published in the issue of Nature Communications. (ANI)