{"id":1512,"date":"2018-03-20T13:47:35","date_gmt":"2018-03-20T17:47:35","guid":{"rendered":"http:\/\/parkinsonpost.com\/?p=1512"},"modified":"2018-03-20T13:47:35","modified_gmt":"2018-03-20T17:47:35","slug":"recruiting-the-brains-underdogs","status":"publish","type":"post","link":"https:\/\/archiveparkinson.thedev.ca\/fr\/recruiting-the-brains-underdogs\/","title":{"rendered":"Recruiting the brain\u2019s underdogs"},"content":{"rendered":"
\"\"

Natalina Salmaso,
Carleton University<\/span><\/p><\/div>\n

About half of the human brain is made up of cells, known as astrocytes, which researchers used to think were like the scaffolding that holds the more important neurons together.<\/p>\n

But Natalina Salmaso knows better. She calls astrocytes the underdogs of the brain: a dynamic class of cells that are just as busy as neurons, but whose work historically went unrecognized. Her research involves revealing how these cells help our brains stay at their best.<\/p>\n

Salmaso, who holds the Canada Research Chair in Behavioural Neurobiology at Carleton University, has spent much of her career studying astrocytes, although not in the context of Parkinson\u2019s disease. She was intrigued when she learned that a lot of the research on this disorder had dealt with astrocytes.<\/p>\n

\u201cAstrocytes go to the neurons when they are dying,\u201d she says. \u201cWhen this happens in Parkinson\u2019s disease, the astrocytes are gathering around them, they\u2019re changing their shape, and they\u2019re emitting different biochemical factors. People have noted these changes are occurring, but no one has really investigated what it means.\u201d<\/p>\n

Now, having received a one-year Pedaling for Parkinson\u2019s Pilot Project Grant through the Parkinson Canada Research Program, Salmaso is going to stimulate astrocytes to learn how they confront the impact that Parkinson\u2019s has on neurons. To do that, she\u2019ll use a virus that has been genetically modified to be sensitive to light, which will interact with astrocytes in a controlled fashion.<\/p>\n

\u201cThe idea is to understand what the stimulation does,\u201d she says. \u201cWe believe the astrocytes are trying to heal the neurons, but failing for some reason. At a molecular level, we want to target what they need to do to heal those neurons earlier in the game.\u201d<\/p>\n

Salmaso believes that targeting astrocytes is akin to using probiotics, which enhance the body\u2019s innate capacity to stay healthy. In the case of Parkinson\u2019s, astrocytes may be trying to do the same. But Salmaso thinks they\u2019re overwhelmed by the amount of inflammation and cell death that has already occurred in the brain. If she can prove that theory, it will set researchers on a path to discovering other mechanisms to help the astrocytes succeed at their job.<\/p>\n

\u201cThe more we understand about how these cells do their job to keep neurons healthy, the more we can mimic that in any model of 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<\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":"

About half of the human brain is made up of cells, known as astrocytes, which researchers used to think were … En savoir plus<\/a><\/p>\n","protected":false},"author":37,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":[],"categories":[237],"tags":[],"yoast_head":"\nRecruiting the brain\u2019s underdogs - Parkinson Canada<\/title>\n<meta name=\"robots\" content=\"noindex, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<meta property=\"og:locale\" content=\"fr_FR\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Recruiting the brain\u2019s underdogs - Parkinson Canada\" \/>\n<meta property=\"og:description\" content=\"About half of the human brain is made up of cells, known as astrocytes, which researchers used to think were ... 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