\ Advocacy \ Doctoral Award Recipients Chosen for Passion and Innovation
To encourage cutting edge research, the ALS Society of Canada – CIHR INMHA Doctoral Research Award was created to fund PhD students conducting ALS-related research for up to three years. This year’s recipients are Xiaoyang Shan and David Gosselin.
Xiaoyang Shan obtained his MD from Guangxi Medical University in China and moved to Canada to pursue graduate studies. He was introduced to neurodegenerative diseases by respected ALS researcher Dr. Charles Krieger while earning his M.Sc. at Simon Fraser University (SFU). Shan is currently a PhD candidate in the department of molecular biology and biochemistry at SFU under the supervision of Dr. David Vocaldo. His research project is entitled “The role of O-glycosylation in a mouse model of ALS.”
Shan notes there is significant evidence that phosphate groups are attaching to proteins in the nervous systems of people with ALS. Because phosphate groups regulate protein action, having too many can interfere with the normal function of proteins. Neurofilaments, proteins associated with the progression of ALS, are known to have excess phosphate in the pathology of ALS and mutant SOD1 mouse models.
Sugar groups may also attach to some of the same sites as the phosphate groups. Scientists speculate that if the sugars can attach to proteins in place of phosphates, the function of some proteins may be improved. Shan believes that achieving a balance between the sugars and phosphates will prevent the accumulation of neurofilaments. He focuses on mouse models of ALS, where he examines the effects of sugar-increasing compounds on various proteins. Initial results have indicated a significant increase in short-term protein levels using one of the compounds. He will next examine if the attachment of phosphates on disease-associated proteins is decreased. This will be followed by a long-term trial to evaluate the effects of the compounds on the progress of ALS. Shan hopes the results will lead to a cure or effective treatment for ALS.
“ALS is a devastating disease affecting thousands of Canadians beyond the approximately 2,500 living with the disease. Finding a cure through research would not only benefit people with ALS, but their families and our society, too,” says Shan.
After obtaining his M.Sc. in physiology and endocrinology at l’Université Laval, David Gosselin is continuing his studies in that department as a PhD candidate under the supervision of Dr. Serge Rivest. His research project is entitled “Increasing microglial expression of CCR2 and IGF-1 through genetic engineering of hematopoietic stem cells (HSC) for the treatment of ALS.”
According to Gosselin, recent studies indicate that mutant SOD1 can activate microglia, the immune cells of the central nervous system. Giving ALS mice immune cells that are unable to be properly activated because of expression of mutant SOD1 accelerates the progression of the disease. The mice will be treated with insulin-like growth factor (IGF-1), which is reported to prolong the lives of SOD1 mice and delay disease progression. IGF-1 will be transmitted to the central nervous system via stem cells isolated from the blood or bone marrow. The cells will also contain CCR2, a chemokine receptor that can improve the ability of immune cells to reach the site of the disease. Chemokine receptors are a small area of protein on the surface of a cell to which external chemical bodies attach. CCR2 is thought to be of central importance to inflammatory diseases and will help IGF-1 attach to the immune cells.
Behavioral tests will be performed to assess recovery, and the central nervous systems of the mice models will be analyzed using markers of inflammation, neurodegeneration and repair. Gosselin believes this proposed therapy will achieve significant results in mouse models of ALS within three or four years and could eventually become a therapeutic treatment for people with ALS.
“I think great progress will be made over the next decade,” says Gosselin. “Researchers are moving beyond studying ALS from a neuronal perspective. We now know enough to realistically attempt to genetically engineer the immune system, which could benefit people living with the disease.”
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Doctoral Award Recipients Chosen for Passion and Innovation
Attracting bright, young investigators to ALS research isn’t an easy task, but through the funding of generous research awards, promising scientists are joining the fight against this devastating disease.To encourage cutting edge research, the ALS Society of Canada – CIHR INMHA Doctoral Research Award was created to fund PhD students conducting ALS-related research for up to three years. This year’s recipients are Xiaoyang Shan and David Gosselin.
Xiaoyang Shan obtained his MD from Guangxi Medical University in China and moved to Canada to pursue graduate studies. He was introduced to neurodegenerative diseases by respected ALS researcher Dr. Charles Krieger while earning his M.Sc. at Simon Fraser University (SFU). Shan is currently a PhD candidate in the department of molecular biology and biochemistry at SFU under the supervision of Dr. David Vocaldo. His research project is entitled “The role of O-glycosylation in a mouse model of ALS.”
Shan notes there is significant evidence that phosphate groups are attaching to proteins in the nervous systems of people with ALS. Because phosphate groups regulate protein action, having too many can interfere with the normal function of proteins. Neurofilaments, proteins associated with the progression of ALS, are known to have excess phosphate in the pathology of ALS and mutant SOD1 mouse models.
Sugar groups may also attach to some of the same sites as the phosphate groups. Scientists speculate that if the sugars can attach to proteins in place of phosphates, the function of some proteins may be improved. Shan believes that achieving a balance between the sugars and phosphates will prevent the accumulation of neurofilaments. He focuses on mouse models of ALS, where he examines the effects of sugar-increasing compounds on various proteins. Initial results have indicated a significant increase in short-term protein levels using one of the compounds. He will next examine if the attachment of phosphates on disease-associated proteins is decreased. This will be followed by a long-term trial to evaluate the effects of the compounds on the progress of ALS. Shan hopes the results will lead to a cure or effective treatment for ALS.
“ALS is a devastating disease affecting thousands of Canadians beyond the approximately 2,500 living with the disease. Finding a cure through research would not only benefit people with ALS, but their families and our society, too,” says Shan.
After obtaining his M.Sc. in physiology and endocrinology at l’Université Laval, David Gosselin is continuing his studies in that department as a PhD candidate under the supervision of Dr. Serge Rivest. His research project is entitled “Increasing microglial expression of CCR2 and IGF-1 through genetic engineering of hematopoietic stem cells (HSC) for the treatment of ALS.”
According to Gosselin, recent studies indicate that mutant SOD1 can activate microglia, the immune cells of the central nervous system. Giving ALS mice immune cells that are unable to be properly activated because of expression of mutant SOD1 accelerates the progression of the disease. The mice will be treated with insulin-like growth factor (IGF-1), which is reported to prolong the lives of SOD1 mice and delay disease progression. IGF-1 will be transmitted to the central nervous system via stem cells isolated from the blood or bone marrow. The cells will also contain CCR2, a chemokine receptor that can improve the ability of immune cells to reach the site of the disease. Chemokine receptors are a small area of protein on the surface of a cell to which external chemical bodies attach. CCR2 is thought to be of central importance to inflammatory diseases and will help IGF-1 attach to the immune cells.
Behavioral tests will be performed to assess recovery, and the central nervous systems of the mice models will be analyzed using markers of inflammation, neurodegeneration and repair. Gosselin believes this proposed therapy will achieve significant results in mouse models of ALS within three or four years and could eventually become a therapeutic treatment for people with ALS.
“I think great progress will be made over the next decade,” says Gosselin. “Researchers are moving beyond studying ALS from a neuronal perspective. We now know enough to realistically attempt to genetically engineer the immune system, which could benefit people living with the disease.”
| Posted On: Thursday, October 25, 2007 Modified: Friday, February 29, 2008 Category: Advocacy Posted By: |