Cécile Voisset Inserm Researcher, PhD, HDR

Course and current status

From 2017      INSERM RESEARCHER (CR1), INSERM UMR1078, SCHOOL OF MEDICINE, IBRBS, UBO UNIVERSITY, BREST, FRANCE.

- Research project: Mechanisms underlying the propagation of infectious amyloid proteins in prion diseases (Creutzfeldt-jakob diseases) and prion-like diseases (e.g., Parkinson's, Alzheimer's and Huntington's diseases)

- Lab director: Emmanuelle Génin

2010-2016      INSERM RESEARCHER (CR1), INSERM UMR1078, SCHOOL OF MEDICINE, UBO UNIVERSITY, BREST, FRANCE.

- Research projects:

  • molecular mechanisms of prion diseases.

  • Identification of molecules able to specifically induce the death of cancer cells infected with Epstein-Barr virus (EBV).

- Lab director: Claude Férec

2007-2010       POST-DOCTORAL FELLOW, INSERM U613, SCHOOL OF MEDICINE, UBO UNIVERSITY, BREST, FRANCE.

- Research projects:

  • molecular mechanisms of prion diseases.

  • Identification of molecules able to specifically induce the death of cancer cells infected with Epstein-Barr virus (EBV).

- Funding: young researcher grant, Inserm

- Lab director: CLaude Férec

2003-2007       POST-DOCTORAL FELLOW, CNRS-UMR8161, INSTITUT DE BIOLOGIE DE LILLE – INSTITUT PASTEUR DE LILLE, FRANCE.

- Research project: Hepatitis C virus entry

- Funding: CNRS, ANRS

- Lab director: Jean Dubuisson

1999-2002      POST-DOCTORAL FELLOW, UNIVERSITY COLLEGE LONDON, WOHL VIRION CENTRE, LONDRES, UNITED KINGDOM.

- Research project : characterization of a new retrovirus isolated from patients with autoimmune diseases (Sjögren’s syndrome ; rheumatoid arthritis)

- Funding : Abbott laboratories, USA

- Lab director: Robin Weiss

1994-1999      PhD STUDENT, CNRS-bioMérieux LABORATORY, LYON, FRANCE.

- Research project : involvement of the new human endogenous retrovirus HERV-W in multiple sclerosis etiology

- Funding: Mérieux Foundation

- PhD director: Glaucià Paranhos-Baccalá

Scientific summary

Prions (PrPSc) are intrinsic components of our cells that rely on cell pathways to spread their infectious conformations. There is a growing number of evidence that other neurodegenerative protein misfolding diseases like Alzheimer’s, Parkinson’s and Huntington’s diseases share key biophysical and biochemical characteristics with prionopathies. However, the molecular mechanisms of propagation of the pathological conformation of the proteins associated to these pathologies are still unknown. Our understanding of these spreading mechanisms is likely to be the key to developing innovative and effective therapeutic strategies.

Hence, our research projects aim at characterizing new therapeutic targets to overcome the propagation of the misfolded protein associated to human neurodegenerative prion-like diseases.

Our research projects involve a large network of national and international collaborations.

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