{"id":1305,"date":"2017-07-17T12:02:43","date_gmt":"2017-07-17T16:02:43","guid":{"rendered":"http:\/\/parkinsonpost.com\/?p=1305"},"modified":"2017-07-17T12:02:43","modified_gmt":"2017-07-17T16:02:43","slug":"helping-cells-cope-with-stress","status":"publish","type":"post","link":"https:\/\/archiveparkinson.thedev.ca\/fr\/helping-cells-cope-with-stress\/","title":{"rendered":"Helping cells cope with stress"},"content":{"rendered":"
\"Jungwoo

Jungwoo Yang<\/p><\/div>\n

Proteins are essential to keeping our bodies\u2019 billions of cells alive and healthy. In order for various proteins to go about their business, they must be folded into specific shapes to interact with other biochemical agents. When that folding fails to occur, or proteins fold themselves into the wrong shapes, trouble arises.<\/p>\n

Jungwoo Yang studies that trouble, which may be among the most fundamental causes of Parkinson\u2019s disease. Yang, a doctoral student at the University of Alberta, is examining a stress response that occurs in a part of the cell known as the endoplasmic reticulum, where tube-like structures deliver proteins to other parts of the cell. When too many of these proteins are unfolded or misfolded, the resulting stress activates an unfolded protein response (UPR) that can damage cells. This response includes a process called phosphorylation of PERK, the addition of phosphates that can eventually poison a cell and kill it.<\/p>\n

\u201cI already knew that this process was happening of higher phosphorylated PERK in people with Parkinson\u2019s disease,\u201d says Yang.<\/p>\n

PERK is the enzyme at the heart of this fatal cascade. Yang began his research by studying how the genetic activation of PERK decides the fate of cells during the stress response within the endoplasmic reticulum. The process resembles the way in which prions cause misfolding of proteins within brain cells, creating the condition known as mad cow disease. Yang suspects a similar culprit might be at work in causing changes within PERK.<\/p>\n

Now, thanks to a two-year, $100,000 Basic Research Fellowship from the Parkinson Canada Research Program, Yang is exploring the possibility that inhibiting PERK\u2019s activity could prevent it from starting the chain of events that kills cells, which in turn could prevent the neurodegeneration seen in Parkinson\u2019s, Alzheimer\u2019s disease or amyotrophic lateral sclerosis (ALS). Yang will test this hypothesis by confirming the mechanism in mice.<\/p>\n

\u201cWe\u2019re going to inject them with endoplasmic reticulum stress inducers and observe the effects of P-PERK inhibitor,\u201d says Yang. \u201cIf we see something that looks like Parkinson\u2019s and inhibits or delays Parkinson\u2019s by using P-PERK inhibitor; that will confirm our model.\u201d<\/p>\n

Eventually, Yang hopes his research will open the way to a drug or gene therapy that could treat or prevent Parkinson\u2018s disease by preventing the stress response that damages or kills brain cells.<\/p>\n

\u201cIf we can inhibit the activity of PERK, it will make a crucial contribution to protecting patients from neurodegeneration. Our study will validate a target mechanism for doing just that as we develop future treatment strategies.\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":"

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