Benjamin DEHAY
  • E-mail :[email]
  • Phone : +33 (0)5 33 51 47 95
  • Location : Bordeaux, France
Last update 2017-10-29 11:01:50.782

Benjamin DEHAY PhD Principal Investigator

Course and current status

2017-present      INSERM Principal Investigator (1st class Researcher), Institute of Neurodegenerative Diseases (Dr. Erwan Bezard) - CNRS UMR 5293 and University of Bordeaux, France.

2013-2017         INSERM Principal Investigator (2nd class Researcher), Institute of Neurodegenerative Diseases (Dr. Erwan Bezard), CNRS UMR 5293 and University of Bordeaux, France.

2010-2013         Senior Post-Doctoral Fellow, in Pathophysiology of Parkinsonian Syndromes Lab (Dr. Erwan Bezard), Institute of Neurodegenerative Diseases, Bordeaux, France. Role of the lysosomal dysfunction during aging, and its implication for Parkinson’s disease

2007-2009         Junior Post-Doctoral Fellow, in Neurodegenerative Diseases Research Lab (Dr. Miquel Vila), Research Institute of the University Hospital Vall d'Hebron, Barcelona, Spain.  Programmed Cell Death and role of intracytoplasmic neuronal inclusions in Parkinson’s disease.  

2003-2007         PhD fellowhip, in CNRS-UMR8541 (Dr. Anne Bertolotti’s team), University of Paris VI, Ecole Normale Supérieure, Paris, France. Modulation of polyglutamine aggregation: subcellular localisation and role of cis-sequences.

Scientific summary

Neurodegenerative diseases represent some of the greatest challenges for basic science and clinical medicine because of their prevalence, cost, complex biochemistry and pathology, and lack of mechanism-based treatments. Parkinson’s disease (PD) is characterized by a progressive accumulation and propagation of α-synuclein likely responsible for their subsequent death. Epidemiological and clinical evidences strongly suggest that PD results from a multifactorial etiology involving both genetic susceptibility factors and environmental exposures superimposing upon aging, the major risk factor for PD. Such multifactorial nature of the degenerative causes and processes has been overlooked so far, explaining the failure in truly replicating PD in mammals. A likely mechanism linking these diseases relates to a lysosomal impairment. In particular, lysosomal defects could potentially account not only for neuronal cell dysfunction/death, the presence of α-synuclein-containing Lewy bodies, but also for promoting the progressive spreading of synucleinopathy. My main goal is to understand how the disease proteins cause alterations of the proteolytic pathways contributing to the pathogenesis for then proposing adapted therapeutic approaches to clear the toxic proteins and halt the disease process. Combining all my knowledge and expertise and taking advantage on a collaborative network, I have initiated a new program of research that will employ a wide range of techniques in complementary fields from cell biology of proteinopathies to animal experimentation to tackle the project with the help of large technologic tools.

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