{"id":1159,"date":"2017-02-13T12:03:44","date_gmt":"2017-02-13T17:03:44","guid":{"rendered":"http:\/\/parkinsonpost.com\/?p=1159"},"modified":"2017-02-13T12:03:44","modified_gmt":"2017-02-13T17:03:44","slug":"preventing-brain-cells-from-running-out-of-fuel","status":"publish","type":"post","link":"https:\/\/archiveparkinson.thedev.ca\/fr\/preventing-brain-cells-from-running-out-of-fuel\/","title":{"rendered":"Preventing brain cells from running out of fuel"},"content":{"rendered":"
\"Dr.

Dr. Wei Yi<\/p><\/div>\n

Most of our body\u2019s cells contain mitochondria, small components crucial to ensuring that a cell obtains adenosine triphosphate (ATP), a molecule that provides essential chemical energy for biological functions. When mitochondria are damaged, a cell must remove them before they contaminate it, which can lead to cell death.<\/p>\n

\u201cIt\u2019s really important to get rid of these mitochondria so that the cell can continue to make use of ATP,\u201d says Wei Yi, a post-doctoral fellow at McGill University\u2019s Montreal Neurological Institute. \u201cIt\u2019s a question of making the most of this vital resource.\u201d<\/p>\n

Wei Yi was recently awarded a two-year, $80,000, Basic Research Fellowship from Parkinson Canada Research Program. Yi\u2019s research focuses on how damaged mitochondria are handled by neurons carrying dopamine, the complex agent that codes signals for movement control in the brain.<\/p>\n

She developed an interest in neurodegenerative diseases like Parkinson\u2019s while studying for her PhD at the Chinese Academy of Sciences.\u00a0 \u201cI am also interested in the aging population of China, where larger numbers of people are likely to be affected by these diseases.\u201d<\/p>\n

Like other cells, neurons regularly remove all kinds of waste material, including mitochondria. This process, known as autophagy, is a rapidly expanding frontier in many areas of medicine. In the case of damaged mitochondria, an enzyme called PINK1 identifies and isolates these components in preparation for disposal. However, in as many as half of patients suffering from early onset Parkinson disease, PINK1 is itself damaged. It can no longer direct the removal of mitochondria.<\/p>\n

\u201cWhen this happens PINK1 is not actually protecting the cells,\u201d Yi says. \u201cThey can end up with bad mitochondria and they will die from a lack of energy.\u201d<\/p>\n

As part of learning more about this problem, her research has revealed another enzyme, called MPP, which appears to control PINK1.<\/p>\n

\u201cBy understanding this mechanism, we can find the pathways that could activate them again,\u201d she explains. \u201cIf we can determine the relationship between PINK1 and MPP, it will provide a new way of treating Parkinson disease.\u201d<\/p>\n

Read about other researchers<\/a> recently funded by the Parkinson Canada Research Program by visiting the research section of archiveparkinson.thedev.ca.<\/p>\n","protected":false},"excerpt":{"rendered":"

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