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Remise du prix Cino Del Duca 2016 pour Erwan Bézard

Le 8 juin 2016

Le Prix scientifique, d’un montant de 275 000 euros est destiné à récompenser une équipe de chercheurs scientifiques français ou étrangers. En 2016, le thème retenu au titre des disciplines de la 2e division est : "Maladies neurodégénératives".

Ce mercredi 8 juin 2016, dans le cadre de la séance solennelle de remise des Grands Prix des Fondations de l’Institut de France, les Grands Prix 2016 de la Fondation Simone et Cino Del Duca ont été attribués. Cet événément, qui a eu lieu sous la coupole de l’Institut de France, est organisé chaque année depuis 2005.

Le Dr Erwan BEZARD (représenté par le Dr Benjamin Dehay) s’est vu remettre le Grand Prix scientifique 2016 de la Fondation Simone et Cino Del Duca pour le projet de recherche « Identification of the α-SYnuclein toxic Species responsible for synucleinopathies », grand prix qu’il partage avec le Dr Ronald MELKI de l’Institut des Neurosciences Paris-Saclay CNRS UMR 9197 de l’Université Paris-Sud. Quoique ayant concouru sur des projets différents (mais complémentaires), tous deux collaborent sur ces questions et leurs équipes de recherche se voient ainsi dotées de 137 500€ chacune.


Bezard, INSERM Research Director, has authored or co-authored over 210 professional publications in the field of neurobiology, most of which are on Parkinson's disease and related disorders. Listed in the Top 1% of the most cited neuroscientists (H factor= 62 – Google Scholar), he is known for his work on the compensatory mechanisms that mask the progression Parkinson's disease and on the pathophysiology of levodopa-induced dyskinesia, the intimate mechanisms of cell death in Parkinson’s disease, the modelling of disease progression and the development of new strategies to alleviate symptoms and/or to slow disease progression.

Bezard is the director of a CNRS research unit located in Bordeaux, the Institute of Neurodegenerative Diseases, which features preclinical and clinical researchers working towards development of therapeutic solutions. He is also a Visiting Professor at the China Academy of Medical Sciences (Beijing, China) where he has set-up and manages a non-human primate facility dedicated to Movement Disorders. He serves on the board of international organizations such as the Michael J. Fox Foundation and Parkinson’s UK. He is Associate Editor of Neurobiology of Disease and of Synapse, two leading journals in the field. He serves on the editorial boards of several other neurobiology journals. Besides consulting for several drug companies in the field of movement disorders, he is a non-executive director of Plenitudes Sarl (France), Motac Neuroscience (UK) and Motac Cognition (USA).

 Project title:

Identification of the α-SYnuclein toxic Species responsible for synucleinopathies
Project Acronym ISYS

Past achievement in relationship with the project The team “Pathophysiology of Parkinsonian Syndromes”, headed by Erwan Bézard (N=30 -, works on two main axis, the pathological response to dopamine replacement therapies in parkinsonian syndromes and the understanding of cell death mechanisms in parkinsonian syndromes. The team is at forefront of international research in these two areas, being a leading translational team, featuring the unique capability of translating internally basic science discoveries into clinical practice within a single team. The team is as well the corner stone of the clinical branch of IMN, half of its researchers being deeply involved into its day-to-day activities. The team published since 1st of January 2010, 244 peer-reviewed articles of which over 100 are authored by the team leader.

The past few years were dedicated to the strengthening of the existing team’s organization and to the development of the axis on cell death mechanisms with significant achievements: i) the world-premiere demonstration of toxicity and spreading of α-synuclein pathology using α-synuclein derived from Lewy Bodies of PD patients in mice AND in monkeys (Recasens et al. Ann Neurol 2014) (“Paper of the Year” 2014 award from American Neurological Association), ii) the demonstration of the key pathological role of lysosomal impairment and the hypothesis that Lewy Bodies might form around autophagolysosomes (Dehay et al. PNAS 2012, Dehay et al. Autophagy 2012) and iii) the development of several protective approaches with notably the acidification of lysosomes using nanoparticles to restore the lysosomal function (Bourdenx et al. Autophagy 2016). The team further developed its scientific visibility in the field of Parkinson’s disease and affiliated diseases: successful grant applications to the ANR and European FP7 program, to the Michael J Fox Foundation (USA), huge contribution to the building/opening of the IMNc, the clinical branch of the IMN. The PSP team significantly contributes to the visibility of the Bordeaux neuroscience community, being a core team member of the Laboratory of Excellence (LabEx - BRAIN and extremely active in various activities related to Science: congress organizations, editorial tasks in several leading journals, founding member of the “Maison du Cerveau” devoted to co-elaboration with patient movies, large number of scientific (in prestigious organizations and major scientific meetings) and non-scientific (lay audience) conferences.

Short presentation of research project

As the overall population benefits from increasing lifespan, neurodegenerative disorders have emerged as a critical health concern. The incidence rate of synucleopathies (e.g. Parkinson’s disease, multiple system atrophy and dementia with Lewy bodies) is 22 (per 100,000 person-years) with Parkinson’s disease alone affecting 1.1 million persons in the EU and 6.3 million worldwide.
While drug therapy for symptom management makes up the largest portion of direct health care costs, it accounts for only 10% of total costs as the major costs arise from late stage complications and dramatic impairment of quality of life. Therefore, neuroprotective or neurorestorative strategies that would stop or slow down the yet unrelenting degenerative process are eagerly awaited as they would have a huge impact both on patients’ quality of life and the economic burden for the society.

We here aim at discriminating between similarities and differences associated with alpha-synuclein (alpha-syn) assemblies in different synucleinopathies. Important limitations in our current in vivo experimental models have hampered studies on disease mechanisms and therapeutic intervention. We shall elucidate the cellular specificity and the temporo-spatial development of a-syn pathology that parallels the development of symptoms.
Our objective is to identify the disease-specific species of a-syn involved in cell death in synucleopathies. Similarities and differences between pathologic alpha-syn species should be evaluated relative to (i) pathology status of brain areas for each Braak Stage (pathology affected vs vulnerable vs resilient brain areas), (ii) tropism for distinct neuronal cells and circuits (iii) pathophysiological consequences. We plan to assess qualitatively, quantitatively and spatially protein aggregates propagation and amplification within the central and peripheral nervous system using state-of-the-art biophysically characterized alpha-syn assemblies and multiple models for functional and behavioural characterization.
The ISYS program will establish whether (i) distinct assemblies follow different propagation pathways and exhibit different tropism for defined neuronal cells and circuits, (ii) there is a relationship between vulnerability of different brain areas and distinct alpha-syn assemblies and (iii) propagation, tropism and vulnerability are age-, disease-, and pathology status-dependent.

Institut des maladies neurodégénératives, CNRS UMR 5293, Université de Bordeaux,:
Dernière mise à jour le 13.06.2016