{"id":1429,"date":"2018-01-16T00:03:37","date_gmt":"2018-01-16T05:03:37","guid":{"rendered":"http:\/\/parkinsonpost.com\/?p=1429"},"modified":"2018-01-16T00:03:37","modified_gmt":"2018-01-16T05:03:37","slug":"establishing-a-new-link-between-brain-and-body","status":"publish","type":"post","link":"https:\/\/archiveparkinson.thedev.ca\/fr\/establishing-a-new-link-between-brain-and-body\/","title":{"rendered":"Establishing a new link between brain and body"},"content":{"rendered":"
\"simon

Dr. Simon Wing,
McGill University<\/span><\/p><\/div>\n

A disease of the brain can become a disease of the entire body, as the breakdown of neural pathways often leads to a loss of muscle mass. Dr. Simon Wing, a professor in McGill University\u2019s Department of Endocrinology and Metabolism, is eager to examine this potential connection as it applies to Parkinson\u2019s disease. He has only recently discovered the possibility of such a link, but it could offer a new perspective on some of the most fundamental aspects of this condition.<\/p>\n

\u201cThrough my research over the last 15 years I found a gene that encodes an enzyme that appears to be important in muscle wasting,\u201d he explains. \u201cThis gene is called USP19.\u201d<\/p>\n

Wing was already studying the behaviour of this gene when he was contacted by a U.S. researcher who discovered that USP19 may also be tied closely to a problematic aspect of Parkinson\u2019s disease. At the heart of this problem is a protein called \u03b1-synuclein, which forms clumps of disruptive material within brain cells. Not only does this material interfere with the ability of these cells to produce dopamine, these affected cells also appear to transmit \u03b1-synuclein to other brain cells, so that the disease spreads and causes more disability.<\/p>\n

\u201cOur work is based on a model where Parkinson\u2019s disease spreads because \u03b1-synuclein is transferred from a sick neuron to a healthy neuron,\u201d says Wing, recipient of a one-year $45,000 Porridge for Parkinson\u2019s (Toronto) Pilot Project Grant. \u201cHowever, nobody really knows how \u03b1-synuclein gets out of the neuron.\u201d<\/p>\n

That detail is crucial, because if researchers can identify and block the transmission mechanism, it might be possible to design a treatment to stop \u03b1-synuclein from leaving affected cells \u2013 stopping Parkinson\u2019s in its tracks.\u00a0 Wing\u2019s U.S. colleague was therefore interested in USP19, which appears to serve as a mediator of this process. More importantly, Wing\u2019s laboratory was already home to mice that have been genetically altered to remove USP19.<\/p>\n

\u201cIf we look at our mice that do not have USP19 and so presumably cannot use this pathway to push \u03b1-synuclein out of the neuron, are they protected against the progression of Parkinson\u2019s disease?\u201d asks Wing. If so, then this finding would pinpoint this gene as a valuable target for possible therapies.<\/p>\n

Wing admits that this prospect remains an open question, but one worth exploring because of its novelty and exciting possibilities. He also acknowledges that this foray into Parkinson\u2019s disease has been a learning experience for him, one that has led him to work with some of the top people in the field at the Montreal Neurological Institute.<\/p>\n

\u201cIt could be quite transformative,\u201d he concludes. \u201cThere are groups already working on developing drugs to block USP19. We could be able to move fairly quickly over a few years into clinical trials if our hypothesis is correct.\u201d<\/p>\n

Editor\u2019s note:<\/p>\n

The most recent Porridge for Parkinson\u2019s biennial event was hosted on November 12, 2017 in Toronto, raising in excess of $200,000. Proceeds from this year\u2019s event support four grants through the Parkinson Canada Research Program, in addition to the novel work of Dr. Wing with the USP19 gene, the following researchers and projects will benefit from the support of Porridge for Parkinson\u2019s (Toronto):<\/p>\n