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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271 entries « 1 of 28 »

Skuk D, Tremblay JP

Myotubes Formed De Novo by Myoblasts Injected into the Scar of Myocardial Infarction Persisted for 16 Years in a Patient: Importance for Regenerative Medicine in Degenerative Myopathies.

Journal Article

Stem Cells Transl Med, 8 (3), pp. 313-314, 2019, ISSN: 2157-6564.

| Links:

Skuk D, Tremblay JP

Sarcolemmal Complement Membrane Attack Complex Deposits During Acute Rejection of Myofibers in Nonhuman Primates.

Journal Article

J Neuropathol Exp Neurol, 78 (1), pp. 38-46, 2019, ISSN: 0022-3069.

Abstract | Links:

Pinto M, Zorn KC, Tremblay JP, Desroches J, Dallaire F, Aubertin K, Marple E, Kent C, Leblond F, Trudel D, Lesage F

Integration of a Raman spectroscopy system to a robotic-assisted surgical system for real-time tissue characterization during radical prostatectomy procedures.

Journal Article

J Biomed Opt, 24 (2), pp. 1-10, 2019, ISSN: 1083-3668.

Abstract | Links:

Duchene BL, Cherif K, Iyombe-Engembe JP, Guyon A, Rousseau J, Ouellet DL, Barbeau X, Lague P, Tremblay JP

CRISPR-Induced Deletion with SaCas9 Restores Dystrophin Expression in Dystrophic Models In Vitro and In Vivo.

Journal Article

Mol Ther, 26 (11), pp. 2604-2616, 2018, ISSN: 1525-0016.

Abstract | Links:

Cherif K, Gerard C, Rousseau J, Ouellet DL, Chapdelaine P, Tremblay JP

Increased Frataxin Expression Induced in Friedreich Ataxia Cells by Platinum TALE-VP64s or Platinum TALE-SunTag.

Journal Article

Mol Ther Nucleic Acids, 12 , pp. 19-32, 2018.

Abstract | Links:

Duchene B, Iyombe-Engembe JP, Rousseau J, Tremblay JP, Ouellet DL

From gRNA Identification to the Restoration of Dystrophin Expression: A Dystrophin Gene Correction Strategy for Duchenne Muscular Dystrophy Mutations Using the CRISPR-Induced Deletion Method.

Journal Article

Methods Mol Biol, 1687 , pp. 267-283, 2018, ISSN: 1064-3745.

Abstract | Links:

Hui CW, St-Pierre MK, Detuncq J, Aumailley L, Dubois MJ, Couture V, Skuk D, Marette A, Tremblay JP, Lebel M, Tremblay ME

Nonfunctional mutant Wrn protein leads to neurological deficits, neuronal stress, microglial alteration, and immune imbalance in a mouse model of Werner syndrome.

Journal Article

Brain Behav Immun, 73 , pp. 450-469, 2018, ISSN: 0889-1591.

Abstract | Links:

Skuk D, Tremblay JP

De Novo Circulating Antidonor's Cell Antibodies During Induced Acute Rejection of Allogeneic Myofibers in Myogenic Cell Transplantation: A Study in Nonhuman Primates.

Journal Article

Transplant Direct, 3 (12), pp. e228, 2017, ISSN: 2373-8731.

Abstract | Links:

Skuk D, Tremblay JP

Cell Therapy in Myology: Dynamics of Muscle Precursor Cell Death after Intramuscular Administration in Non-human Primates.

Journal Article

Mol Ther Methods Clin Dev, 5 , pp. 232-240, 2017, ISSN: 2329-0501.

Abstract | Links:

Perrin A, Rousseau J, Tremblay JP

Increased Expression of Laminin Subunit Alpha 1 Chain by dCas9-VP160.

Journal Article

Mol Ther Nucleic Acids, 6 , pp. 68-79, 2017.

Abstract | Links:

271 entries « 1 of 28 »
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Active projects

  • Centre thématique de recherche en neurosciences, Subvention, Institutionnel - BDR, BDR - Centres de recherche reconnus, from 1999-06-01 to 2020-10-18
  • Centres hospitaliers universitaires de Québec - Université Laval, Subvention, Centre hospitalier universitaire de Québec - Université Laval, Centres de recherche affiliés, from 2017-01-01 to 2099-12-31
  • Correction of the dystrophin gene with Zinc Finger Proteins and TAL effector nuclease, Subvention, Instituts de recherche en santé du Canada, Subvention de fonctionnement, from 2012-10-01 to 2020-03-31
  • Deciphering the role of DCIR in HIV-1 pathogenesis, Subvention, Instituts de recherche en santé du Canada, Subvention Projet, from 2018-04-01 to 2023-03-31
  • Development of a treatment of Alzheimer based on the editing of the Amyloid Precuror Protein gene with the CRISPR system., Subvention, Weston Brain institute, Transformational Research, from 2016-01-15 to 2020-01-31
  • Phase I/II clinical trial of myoblast transplantation to Duchenne Muscular Dystrophy patients., Subvention, Instituts de recherche en santé du Canada, Subvention de fonctionnement, from 2013-10-01 to 2020-03-31
  • Utilisation de la technologie CRISPR / Cas9 dans le développement d'un traitement permanent contre la maladie d'Alzheimer, Subvention, Ministère des Relations internationales, de la Francophonie, Coopération Québec-Brésil, from 2018-04-01 to 2020-03-30

Recently finished projects

  • Développement de thérapies géniques pour l'Ataxie de Friedreich, Partenariat, MITACS Inc., Accélération Québec (MITACS et gouvernement provincial), from 2016-12-01 to 2019-01-31
  • Human inducible pluripotent stem cells (IPSC) plateform, Subvention, La Fondation Neuro Canada / Brain Canada, Soutien aux plateformes technologiques (SSPT), from 2015-04-01 to 2018-09-30
Data provided by the Université Laval research projects registery