Jacques P. Tremblay received a B.Sc. in Biochemistry from McGill University in 1970, and a Ph.D. in Neuroscience from UCSD (University of California in San Diego) in 1974. From 1975 to 1976, he was a postdoctoral fellow at the Laboratory of Neurobiology of l’Hôpital de l’Enfant-Jésus. Subsequently, he spent his entire career at Laval University: Professor under grant from 1976 to 1981 in the Department of Anatomy; Assistant Professor from 1981 to 1985; full Professor from 1985; Director of the Department of Anatomy from 1987 to 1997, and Professor of the Department of Molecular Medicine from 2010 to now. He is currently a regular researcher at the Axis of Neuroscience of the CHU Research Center of Quebec-Université Laval.

Development of a treatment for Duchenne Muscular Dystrophy (DMD)

DMD is due to a mutation of the gene coding for the dystrophin protein. This mutation leads to an absence of this protein under the membrane of muscle fibers. His laboratory is renowned for his work on the transplantation of normal allogeneic myoblasts as a treatment for DMD. His Phase I clinical trial for this therapy showed that this transplant restores the expression of this protein in the patient’s muscle fibers. In 2006, Dr. Tremblay received the Henry Friesen Award from the Royal College of Physicians and Surgeons of Canada for his work on this therapy. His group is currently conducting a Phase I / II clinical trial on this therapy. In addition, his group is currently using CRISPR / Cas9 technology to correct the dystrophin gene, creating an additional deletion to produce a hybrid exon of the dystrophy gene, which not only restores the expression of dystrophin but also produces dystrophin with a normal structure.

Development of a treatment for Friedreich’s Ataxia

Dr. Tremblay’s group has also been conducting research on Friedreich’s Ataxia since 2010. This disease is due to an elongation of the GAA trinucleotide repeat in intron 1 of the frataxin gene, which reduces expression of this protein, leading to the death of neurons and cardiomyocytes that induce neurological and cardiac symptoms. His group demonstrated that the expression of frataxin is increased by targeting the promoter of this gene with TALE-VP64 proteins. In addition, it has also demonstrated that it is possible to suppress trinucleotide repetition by cutting with the CRISPR / Cas9 system before and after this repeat.

Development of a treatment for Alzheimer’s disease

This group also uses CRISPR / Cas9 technology to develop a treatment for Alzheimer’s disease. This disease is due to the abnormal metabolism of the APP protein (Amyloid Precursor Protein) which leads to the formation of beta-amyloid peptides that form plaques. The formation of these peptides can be greatly reduced by the A673T mutation of the APP gene observed in a small portion of Iceland’s population. Dr. Tremblay’s group has demonstrated that this mutation could be produced with the CRISPR / Cas9 system.

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Schlapfer WT, Woodson PB, Tremblay JP, Barondes SH

Depression and frequency facilitation at a synapse in Aplysia californica: evidence for regulation by availability of transmitter

Journal Article

Brain Res, 76 (2), 1974.

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Active projects

  • Correction with the Prime editing technology of point mutations responsible for Duchenne Muscular Dystrophy, from 2023-03-01 to 2024-02-29
  • Development of an AAV library, from 2022-04-01 to 2024-03-31
  • Développement d’une thérapie génique pour l’ataxie de Friedreich, from 2021-05-31 to 2023-05-31
  • PRIME editing correction of the T1709M mutation responsible for some cases of Ryanodine receptor type I-related myopathies, from 2021-07-01 to 2023-06-30
  • Removal of the GAA repeat with the CRISPR/Cas9 system in Friedreich patient cells and in the YG8sR mouse model, from 2019-10-01 to 2024-09-30

Recently finished projects

  • Correction by CRISPR base editing of point mutations responsible for Duchenne Muscular Dystrophy, from 2020-06-01 to 2022-05-31
  • Correction of the c. 121 A to T mutation in the NKX6-2 gene by PRIME editing, from 2021-08-23 to 2022-08-22
  • Deciphering the role of DCIR in HIV-1 pathogenesis, from 2018-04-01 to 2023-03-31
  • Development of a rapid and simple test to detect the COVID-19 variants that can be used in remote areas and developing countries, from 2021-06-01 to 2022-05-31
  • Directing cellular identity to move towards progenitor cell therapies, from 2013-04-01 to 2022-03-31
  • Financement d'une bourse visant à corriger une mutation ponctuelle dans le gène DYSF, from 2023-01-09 to 2023-03-31
  • Génération de lignées isogéniques pour les mutations GNA11/BAP1 par « PRIME editing » comme modèles d’études du mélanome oculaire., from 2021-04-01 to 2022-03-31
  • Les cellules souches pluripotentes génétiquement corrigées comme thérapie pour l’epidermolyse bulleuse simplex, from 2022-04-01 to 2023-03-31
  • Phase I/II clinical trial of myoblast transplantation to Duchenne Muscular Dystrophy patients., from 2013-10-01 to 2022-03-31
  • Using extracellular vesicles to deliver therapeutic proteins for various ataxia, from 2020-03-01 to 2021-07-01
  • Utilisation de vésicules extracellulaires pour livrer les composants de la technologie d’édition du génome CRISPR/PRIME, from 2021-04-01 to 2022-03-31
Data provided by the Université Laval research projects registery