Dr. Tremblay is born in Montreal in 1946. He completed a B.A. at college Ste Marie in 1967 and a B.Sc. in Honours Biochemistry at Mc Gill University in 1970. He obtained in 1974 a Ph.D. in Neuroscience from the University of California in San Diego (UCSD). He is a professor at Laval University since 1976 and a full professor since 1985. He was the chairman of the department of Anatomy from 1987 to 1997.
Dr. Tremblay has published 183 articles in peer reviewed journals and presented 304 communications in congress. He has presented 75 invited conferences in international congress.
The aim of Dr. Tremblay laboratory is to develop a treatment for recessive muscular dystrophies, particularly Duchenne Muscular Dystrophy (DMD), Becker Muscular Dystrophy and Hereditary Inclusion Body Myopathies (HIBM) based on the transplantation of allogeneic normal or autologous genetically corrected muscle precursor cells (myoblasts).
The research conducted by Dr. Tremblay team has permitted excellent transplantation results in animal models. In dystrophic mice, the transplantation of myoblasts has restored the expression of dystrophin in 95% of the muscle fibers. More than 30,000 muscle fibers expressed a reporter gene following the transplantation of genetically modified myoblasts throughout the biceps of monkeys immunosuppressed with Tacrolimus (Prograft). This success permitted to this team to obtain the permission from Health Canada to do a phase I clinical trial of myoblast transplantation to DMD patients. Dystrophin expression was observed in the muscle fibers of eight of the nine patients who received myoblast transplantation during this clinical trial. His team has recently obtained the permission to undertake a follow-up clinical trial to verify whether the transplantation of normal myoblasts throughout one arm muscle can increase the strength of that muscle.
Cellular therapy has evolved since the first blood transfusion. Using specialized techniques, it has been possible to recognize and isolate the cells responsible of the repair of particular tissues like muscles. It is actually possible to isolate these “satellite cells” from a healthy donor and then to culture them in laboratory. Placing only one “satellite cells” in adequate specific medium and providing it the necessary nutrients, we can obtain more than ten millions after one month of culture! These cells can be transplanted to repair damaged muscles.
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Duchenne muscular (DMD) is an X-linked recessive genetic disease caused by mutations in dystrophin gene leading to a missing or non functional dystrophin protein. DMD is thus produced by a severe deficiency of dystrophin, a protein located under the membrane of the muscle fiber, that connects the contractile proteins with a complex of proteins located in the membrane. The presence of dystrophin protects the muscle fiber membrane during contraction.
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Early signs of Duchenne Muscular Dystrophy, which, usually occur between the ages of 2 and 6, include frequent falling, difficulty getting up from a sitting or lying position, and a waddling gait. Other hallmarks are difficulty to climb stairs, tip toe walking, shoulder and arm weakness. The pathology is also characterized by the apparent enlargement of the calf and sometimes other muscles, which, is really due to an accumulation of fat and connective tissue in the muscle.
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