lundi, lundi 25 mars 2019
Opening Ceremony 17h30 > 18h45 Cérémonie d'Ouverture Amphi A
18h00 S01-01 Cérémonie d'Ouverture > A. Axel MARCHAL (Bordeaux, France)
mardi mardi 26 mars 2019
26-AM-Plenary 09h00 > 10h30 Myologie Translationnelle Amphi A
  • Modérateurs : O. Odile BOESPFLUG-TANGUY (Paris, France), P. Pascal MAIRE (Paris, France)
09h00 S02-01 > F. Frédéric RELAIX (Paris, France) 09h30 S02-02 Approaches to delay the progression of Muscular Dystrophy > G. Graziella MESSINA (Milan, Italy) 10h00 S02-03 Expression and functional analyses of Dlk1 in muscle stem cells and mesenchymal progenitors during regeneration > S-I. So-Ichiro FUKADA (Osaka, Japan)
26-AM-Coffee 10h30 > 11h00 Pause Café & Exhibition (Poster / Stand) Pluriel Room
26-AM-Parallel-1 11h00 > 12h30 Myopathies Congénitales Amphi A
  • Modérateur : A. Ana FERREIRO (Paris, France)
11h00 S03-01 Modulation of amphiphysin and dynamin rescues severe congenital myopathies > J. Jocelyn LAPORTE (Illkirch, France) 11h30 S03-02 > H. Heinz JUNGBLUTH (London, United Kingdom) 12h00 S03-03 > C. Coen Ac OTTENHEIJM (Amsterdam, Netherlands)

Objectif(s) : Causes of many myopathies remain unresolved and succesfull treatment strategies are scarce. A prime example of an unresolved, but life-threatening muscle disease is nemaline myopathy. In muscle cells, the contractile machinery is arranged into sarcomeres, a system of interdigitating thin and thick filaments. Where the thick filament is mainly composed of myosin, the thin filament is composed of an actin backbone decorated with regulatory proteins, such as troponin, tropomyosin and the giant protein nebulin. It is this thin filament that is implicated in nemaline myopathy. Mutations in twelve genes have been indicated to play a role, all genes encoding proteins that are either components of the thin filament or are thought to contribute to stability or turnover of thin filament proteins. It is therefore, that nemaline myopathy is considered a ‘thin filament myopathy’. These mutations in thin filament proteins, together with the crucial role of the thin filament in muscle function, raise the question: is the functioning of the thin filament affected in nemaline myopathy, and if so, how ? Only in recent years this question has been addressed, and many important ones have yet to be answered. Understanding the genotype-phenotype correlations in nemaline myopathy is important, as it allows for the development of genotype-targeted treatment strategies.
26-AM-Parallel-2 11h00 > 12h30 Cardiomyologie Amphi B
  • Modérateur : D. Denis DUBOC (Paris, France)
11h00 S04-01 > K. Karim WAHBI (Lyon, France) 11h30 S04-02 Altered cytoskeleton in cardiac disease caused by nuclear A-type lamins gene mutations > A. Antoine MUCHIR (Paris, France) 12h00 S04-03 > J. John BOURKE (Newcastle, United Kingdom)
26-AM-Symposium 12h30 > 14h00 SYMPOSIUM INDUSTRIE: AVEXIS Amphi C
26-AM-Lunch 12h30 > 14h00 Déjeuner Libre - Exhibition (Poster / Stand) Pluriel Room
  • Modérateur : S. Serge BRAUN (Evry, France)
14h00 S05-01 Small non-coding RNAs of intron origin in Myotonic Dystrophy type 1: new candidate drivers of splicing defects > B. Baptiste BOGARD (Paris, France) 14h15 S05-02 Downregulation of Phosphodiesterase 10A mitigates the manifestation of DMD phenotype in zebrafish model > M. Matthias LAMBERT (Boston, USA) 14h30 S05-03 Using Human Pluripotent Stem Cells Derived Motor Neurons to address the Pathogenesis of Spinal Muscular Atrophy > C. Camille JANUEL (CORBEIL-ESSONNES)

Objectif(s) : Spinal muscular atrophy (SMA) is the most common genetic cause of infant mortality characterized by the specific degeneration of lower motor neurons (MNs) in the spinal cord, leading to progressive paralysis and muscle atrophy. SMA etiology relates to insufficient amount of SMN protein, which results from mutations in the survival motor neuron 1 (SMN1) gene. Despite the ubiquitous expression of SMN protein, it is still unclear why MNs are one of the most affected cell types. Understanding this specific cellular tropism is critical but requires access to the relevant cell type. MNs from mouse are difficult to isolate and are obviously impossible to access from human. The ability to reprogram somatic cells into human induced pluripotent stem cells (hiPSC) offers a unique opportunity to access normal and pathological bona fide neuronal populations in sufficient quantities for systematic molecular and cellular analysis. In this present study, we demonstrated that the reduced expression of SMN led to a decreased survival of hiPSC-derived motoneurons rather than a defect in their generation, phenotype that can be rescued by the reintroduction of SMN protein. We identified that this phenotype can be rescued by kenpaullone, an inhibitor of several CKDs (cyclin-dependent kinases) as well as GSK-3b, likely through a CDK independent mechanism. By a transcriptomic approach on SMA hiPSC-derived MNs, we identified SMA-specific changes in early MNs that include genes involved in synaptic plasticity. Interestingly, these genetic defects were partially rescued by kenpaullone treatment. These findings suggest that alteration in synaptic organization might be a new therapeutic target for SMA. Altogether, our results demonstrate the potential offered by human pluripotent stem cells to shed light on the cellular and molecular bases of selective motor neuron vulnerability in SMA condition.
14h45 S05-04 Genetic control of skeletal muscle fiber type > M. Matthieu DOS SANTOS (Paris, France)
26-PM-Plenary 15h00 > 16h00 Outils d’Évaluation et Biomarqueurs Amphi A
  • Modérateurs : N. Nathalie GOEMANS (Leuven), V. Volker STRAUB (Newcastle, United Kingdom)
15h00 S06-01 > J. Jordi DIAZ-MANERA (Barcelona, Spain) 15h30 S06-02 Identification of prognostic and pharmacodynamic serum biomarkers in Duchenne and Becker muscular dystrophies > P. Pietro SPITALI (Leiden, Netherlands)
26-PM-Coffee 16h00 > 16h30 Pause Café & Exhibition (Poster / Stand) Pluriel Room
26-PM-Parallel-1 16h30 > 18h00 Dystrophies Musculaires des Ceintures et Dystrophies Musculaires Congénitales Amphi A
  • Modérateur : B. Bruno EYMARD (Paris, France)
16h30 S07-01 > I. Isabelle RICHARD (Evry, France) 17h00 S07-02 > C. Carsten BONNEMANN (Washington, USA) 17h30 S07-03 Two in vitro muscular dystrophy modelling approaches for development and verification of gene therapy methods > I. Ivan YAKOVLEV (Moscow, Russia) 17h45 S07-04
26-PM-Parallel-2 16h30 > 18h00 Muscle et Système Nerveux Central Amphi B
  • Modérateurs : F. Francesco MUNTONI (London, United Kingdom), A. Alvaro RENDON (Paris, France)
16h30 S08-01 Genotype-phenotype relationships underlying visual, cognitive and neuropsychiatric disorders in Duchenne muscular dystrophy > F. Francesco MUNTONI (London, United Kingdom) 17h00 S08-02 Neurobehavioral dysfunctions and therapeutic approaches in DMD mouse models lacking brain dystrophins > C. Cyrille VAILLEND (Orsay, France) 17h30 S08-03 Electroretinographic anomalies as biomarkers of CNS dysfunction and for evaluation of gene therapy efficacy: Insights from the preclinical study of Dp71-null mice > J. Jan KREMERS (Erlangen, Germany) 17h45 S08-04 Defective visual information processing in Duchenne muscular dystrophy > D. Dora Fix VENTURA (Sao Paulo, Brazil)
26-PM-Symposium 18h00 > 20h00 SYMPOSIUM INDUSTRIE: SAREPTA Amphi C
mercredi mercredi 27 mars 2019
27-AM-Plenary 09h00 > 10h30 Les leçons à tirer des essais thérapeutiques négatifs Amphi A
  • Modérateur : E. Enrico BERTINI (Rome, Italy)
09h00 S09-01 GNE Myopathy Therapy Trial With Sialic Acid Supplementation: Why did phase 3 'fail'? > Z. Zohar ARGOV (Jerusalem, Israel) 09h30 S09-02 > K. Kathryn WAGNER (Baltimore, USA) 10h00 S09-03 Cell Therapies > J. Jennifer MORGAN (London, United Kingdom)

Objectif(s) : Stem cells have been suggested as a possible treatment for muscular dystrophies, such as Duchenne muscular dystrophy (DMD). This was based on work using pre-clinical animal models of DMD, showing that different muscle stem cells contributed to regenerated muscle fibres following either their local or systemic delivery. The muscle fibres of donor origin expressed dystrophin, which should protect them from undergoing further rounds of necrosis and regeneration. As well as contributing to regenerated muscle fibres, some types of donor stem cell also functionally reconstituted the skeletal muscle stem cell pool, thus providing long-term benefit. The first clinical trials of stem cells in DMD, performed in the 1990s, involved the intra-muscular transplantation of myoblasts derived from normal donors. The outcomes of these and subsequent trials have been disappointing, with little evidence of donor cell engraftment and no significant functional benefit. But findings from these trials and from stem cell transplantation experiments in mouse models, highlight several major hurdles that need to be overcome. The majority of cells die very rapidly following their intra-muscular transplantation and the minority that survive may not proliferate extensively. Also, the transplanted cells do not migrate far from the site of injection. Systemic transplantation of stem cells would be required to treat patient muscles body-wide, but ensuring that they reach, enter and contribute to muscle fibres within downstream muscles are major obstacles. Immune rejection of either the transplanted cells, or the donor-derived muscle fibres that express de novo dystrophin, is another potential problem. This might be circumvented by cell-mediated gene therapy of autologous stem cells, or by genetically-correcting autologous stem cells. Generating sufficient cells for either local or systemic delivery is a further issue. Expansion of skeletal muscle stem cel
27-AM-Coffee 10h30 > 11h00 Pause Café & Exhibition (Poster / Stand) Pluriel Room
27-AM-Parallel-1 11h00 > 12h30 Motoneurone - Jonction Neuromusculaire et Membrane Musculaire Amphi A
  • Modérateur : B. Bruno ALLARD (Lyon, Paris)
11h00 S10-01 Regulation of neuromuscular connectivity by Wnt signaling: from signaling molecule to therapeutic strategies > L. Laure STROCHLIC (Paris, France) 11h30 S10-02 > J-L. Jean-Louis BESSEREAU (Lyon, France) 12h00 S10-03 Sarcolemmal membrane repair activated by conserved intracellular signaling responses can compensate for membrane fragility in muscular dystrophy > N. Noah WEISLEDER (Columbus, USA)

Objectif(s) : A conserved plasma membrane repair mechanism exists to counteract sarcolemmal membrane damage in muscle cells, restore membrane barrier function, and maintain muscle cell homeostasis. Membrane damage induced by various insults requires an effective repair mechanism and any disruption of the process gives rise to several pathophysiological states. Previous studies indicate that compromised repair capacity in striated muscle can lead to muscular dystrophy and that increasing membrane repair capacity can have therapeutic effects in animal models of muscular dystrophy. This membrane repair response can involve various cellular mechanisms to repair large disruptions in the sarcolemmal membrane, including activation of signaling pathways that trigger vesicular trafficking to the site of injury followed by vesicular fusion with the damaged portion of the membrane to patch the membrane disruption. Multiple proteins, including dysferlin, TRIM72/MG53, and various annexins, participate in this repair response. Numerous studies have shown that several aspects of vesicle trafficking are dependent on the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) signaling pathway. In this study, membrane repair assays on skeletal muscle and non-muscle cell lines demonstrated that the membrane repair process is dependent on activation of the PI3K signaling axis through the downstream target Akt1. This signaling response facilitates the function of TRIM72/MG53 in membrane repair since blocking PI3K or Akt1 minimizes the elevated membrane repair produced by TRIM72/MG53 overexpression. One mechanism found to increase membrane repair following TRIM72/MG53 overexpression or PI3K/Akt1 activation is elevated exocytotic and endocytotic activity. Further, multi-photon microscopy studies indicate that the PI3K/Akt1 pathway is relevant to membrane repair in isolated mouse muscle bundles injured because PI3K or Akt1 inhibition prevents membrane resealing. Dystrophic skeletal muscle and cardiac tis
27-AM-Parallel-2 11h00 > 12h30 Dystrophies Myotoniques Amphi B
  • Modérateur : G. Geneviève GOURDON (Paris, France)
11h00 S11-01 Myotonic dystrophies: current core clinical phenotypes > G. Giovanni MEOLA (Milano, Italy)

Objectif(s) : 1 Describe the current core clinical phenotypes in DM1 and DM2 2 Overview the muscular and extra muscular symptoms in myotonic dystrophies (DMs) 3 Describe for both subtypes the overlapping and differences in myotonic dystrophies
11h30 S11-02 RNA-based approaches to reverse repeat expansion toxicity in Myotonic Dystrophy > D. Denis FURLING (Paris, France) 12h00 S11-03 3D reconstruction of DM1 patients’ myoblasts: studying the relationship between CTG repeats, RNA foci and MBNL1 in single cells > A. Alfonsina BALLESTER-LOPEZ (Badalona, Spain)
27-AM-Symposium 12h30 > 14h30 SYMPOSIUM INDUSTRIE: BIOGEN Amphi C
27-AM-Lunch 12h30 > 14h30 Déjeuner Poster Pluriel Room
27-PM-Plenary 14h30 > 16h00 Thérapies Géniques Amphi A
  • Modérateurs : S. Serge BRAUN (Evry, France), G. Giuseppe RONZITTI (Evry, France)
14h30 S12-01 > K. Kevin FLANIGAN (Columbus, USA) 15h00 S12-02 Optimization of AAV-mediated gene therapy for SOD1-linked ALS > M-G. Maria-Grazia BIFERI (Paris, France) 15h30 S12-03 > A. Anna BUJ-BELLO (Evry, France)
27-PM-Coffee 16h00 > 16h30 Pause Café & Exhibition (Poster / Stand) Pluriel Room
27-PM-Parallel-2 16h30 > 18h00 Du muscle en développement au muscle vieillissant Amphi A
  • Modérateur : G. Gillian BUTLER-BROWNE (PARIS)
16h30 S14-01 > S. Shahragim TAJBAKHSH (Paris, France)

Objectif(s) : Regulation of skeletal muscle stem cells during homeostasis and regeneration involves the interplay between extrinsic and intrinsic cues. In a series of studies, we investigated Notch as a key mediator of muscle stem cell stability and fate through extrinsic regulation of extracellular matrix, and internal regulation of cell migration via the mirtron mir708. Using static and live imaging, these observations led us to propose a two-step mechanism where the final mitosis before cellular quiescence, and cell migration, are negotiated before niche occupancy. Using cell lineage reporter mice, our data show that muscle stem cells exit from the cell cycle first, continue to migrate, then arrest and occupy the niche under the regulation of two Notch mediated axes. In parallel, we developed a novel in vivo clonal cell lineage method using Pax7 reporter mice to mark all muscle stem cells, and combined this with transcription factor readouts (Pax7, MyoD and Myogenin as stem and differentiating markers) to assess division asymmetry. Our ex vivo live imaging of artificial niches on fibronectin coated micropatterns, and in vivo clonal analyses show for the first time that asymmetric and symmetric cell divisions both contribute to the self-renewal process in vivo. This division asymmetry was examined in more detail using H3.1-SNAP transgenic mice that we generated that allow tracking of old and new histone pools. Using this transgenic in combination with clonal lineage studies in vivo, we show that in contrast to the fly germ line where this histone variant was reported to segregate asymmetrically, we observe symmetric distribution of H3.1 during muscle stem cell asymmetric cell divisions. Taken together, we show that muscle stem cell regulation is dynamic during homeostasis and regeneration and we propose a model of how the asymmetry apparatus engages in cell fate decisions during muscle stem cell self-renewal and differentiation during tissue regeneration.
17h00 S14-02 Recovery macrophages secrete pro-fusogenic effectors during skeletal muscle regeneration > B. Bénédicte CHAZAUD (Lyon, France) 17h30 S14-03 Dynamics of muscle growth, regeneration and hypertrophy provide an essential quantitative basis to understanding muscle stem cell function > T. Terence PARTRIDGE (Washington, USA) 17h45 S14-04 Attenuation of myostatin/activin signaling delay aging signs in progeric mice model > K. Khalid ALYODAWI (Reading, United Kingdom)
27-PM-Parallel-1 16h30 > 18h00 La lutte contre l'errance diagnostique Amphi B
  • Modérateur : E. Emmanuelle LAGRUE (Tours, France)
16h30 S13-01 Targeted therapies for rare neuromuscular disorders – first steps towards a treatabolome > H. Hanns LOCHMULLER (Ottawa, Canada) 17h00 S13-02 Genetic Landscape of Limb Girdle Muscular Dystrophies > M. Madhuri HEGDE (Waltham, USA)

Objectif(s) : 1. Understanding the diagnostic yield from genetic testing 2. Genetic heterogeneity - from single gene to multigene contribution 3. Whole Genome Sequencing in neuromuscular disorders
17h30 S13-03 Spinal Muscular Atrophy : A challenging disease for Newborn screening ? > L. Laurent SERVAIS (Liège, Paris)
27-PM-Symposium 18h00 > 19h30 SYMPOSIUM INDUSTRIE: AKCEA Amphi C
jeudi jeudi 28 mars 2019
28-AM-Plenary 09h00 > 10h30 Thérapies à l'Horizon Amphi A
  • Modérateur : J-M. Jean-Marie GILLIS (Brussels, Belgium)
09h00 S15-01 > M. Matthew WOOD (Oxford, United Kingdom)

Objectif(s) : Oligonucleotide therapies for neuromuscular disease Gene based therapeutic interventions have the potential to transform the treatment landscape for neuromuscular diseases. After more than a decade of effort, significant progress has been made in the development of first generation oligonucleotide therapies for Duchenne muscular dystrophy (DMD) and spinal muscular atrophy (SMA). These oligonucleotide drugs modulate target gene splicing in order to correct the underlying genetic defect and restore expression of essential proteins. First generation oligonucleotides, while demonstrating proof-of-principle, suffer from the limitation of inadequate tissue and cell delivery - the major barrier to the development of potent, disease modifying oligonucleotide interventions. The goal of second generation oligonucleotides is to overcome the barrier of intracellular delivery either by the development of novel oligonucleotide backbone chemistries with improved delivery properties and/or by exploitation of delivery technologies which may be coupled with oligonucleotide drugs.
09h30 S15-02 Tamoxifen as a treatment for muscular diseases: an unexpected facet of a repurposed anticancer drug > O. Olivier DORCHIES (Geneva, Switzerland) 10h00 S15-03 Vamorolone retains efficacy and reduces safety concerns of glucocorticoid drugs > E. Eric HOFFMAN (Rockville, USA)
28-AM-Coffee 10h30 > 11h00 Pause Café & Exhibition (Poster / Stand) Pluriel Room
28-AM-Parallel-1 11h00 > 12h30 Dystrophie musculaire Facio-Scapulo-Humérale Amphi A
  • Modérateur : S. Sabrina SACCONI (Nice, France)
11h00 S16-01 > S. Silvere VAN DER MAAREL (Leiden, Netherlands)

Objectif(s) : Facioscapulohumeral dystrophy (FSHD) is one of the most common inherited myopathies clinically defined by progressive weakness and wasting of the facial, shoulder girdle and upper arm muscles. With disease progression, other muscles may become affected too. Non-muscular features are rare, and often subclinical. FSHD is associated with inappropriate expression of the cleavage stage transcription factor DUX4 as a consequence of partial chromatin relaxation of the D4Z4 repeat on chromosome 4q35. The D4Z4 repeat varies between 8-100 units in the population and adopts a repressive chromatin structure in somatic cells such as skeletal muscle. As a result of D4Z4 repeat contractions to a size of 1-10 units (FSHD1), or mutations in chromatin modifiers that facilitate a repressive D4Z4 chromatin structure in somatic cells (FSHD2), in FSHD muscle the D4Z4 chromatin structure is more relaxed. This causes derepression of the D4Z4-embedded DUX4 retrogene in skeletal muscle, which, in turn, initiates a cascade of events leading to muscle damage. Most FSHD2 patients have a heterozygous mutation in SMCHD1 encoding a chromatin repressor that binds to D4Z4. Reduced SMCHD1 repressor activity at D4Z4 causes DUX4 expression in skeletal muscle. SMCHD1 was also identified as a modifier for FSHD1 and a recent FSHD population study suggests that, rather than separate entities, FSHD1 and FSHD2 form a continuum in which genetic (the repeat size) and epigenetic (the activity of D4Z4 chromatin modifiers) synergistically contribute to DUX4 derepression and disease presentation. Only a minority of myonuclei express DUX4 in FSHD muscle cell cultures. How such sporadic expression leads to severe muscle wasting in FSHD largely remains unclear. Indeed transcriptome studies in FSHD have systematically been challenged by the sporadic nature of DUX4 expression, with the majority of non-affected cells masking the consequences of the presence of DUX4. Taking advantage of single-cell RNA-sequencing, comb
11h30 S16-02 Applying genome-wide CRISPR screens for therapeutic discovery in FSHD > A. Angela LEK (New Haven, USA) 12h00 S16-03 PAX7, DUX4 and Facioscapulohumeral muscular dystrophy > P. Peter ZAMMIT (London, United Kingdom)

Objectif(s) : Skeletal muscle is an archetypal adult stem cell model, in which maintenance, growth and repair of functionally specialised post-mitotic cells is achieved by recruitment of undifferentiated precursors. For the past 18 years, my core research has been directed at understanding how muscle stem cells are regulated in healthy, aged and diseased skeletal muscle. The functional unit of skeletal muscle is the myofibre: a giant syncytial cell maintained by hundreds of post-mitotic myonuclei. The routine needs for myonuclear homeostasis, together with the more sporadic demands for hypertrophy and repair, are performed by muscle satellite cells. These resident stem cells are normally mitotically quiescent in mature muscle, and so must first be activated to undergo extensive proliferation to generate myoblasts that eventually differentiate to provide new myonuclei. The main themes of the group at King’s College London currently include investigating the transcriptional and signaling control of satellite cell activation and cell fate choice, and examining pathomechanisms and potential therapies for Emery-Dreifuss muscular dystrophy, Fascioscapulohumeral muscular dystrophy and rhabdomyosarcoma.
28-AM-Parallel-2 11h00 > 12h30 Glycosylation / Sialisation Amphi B
  • Modérateur : C. Cecilia JIMENEZ-MALLABRERA (Esplugues De Lobregat, Spain)
11h00 S17-01 Glycosylation and sialylation in congenital muscular diseases: the glycobiologist’s point of view > A. Arnaud BRUNEEL (Paris, France)

Objectif(s) : Dresser un "état des lieux" non-exhaustif des liens entre les anomalies de la glycosylation/sialylation et les maladies musculaires congénitales.
11h30 S17-02 Molecular mechanisms involved in MDC1A / LAMA2 MD and development of possible treatment options > M. Markus RUEGG (Basel) 12h00 S17-03 Genotype-phenotype correlation in GNE myopathy > O. Oksana POGORYELOVA (Newcastle, United Kingdom)
28-AM-Symposium 12h30 > 14h00 INDUSTRY SYMPOSIUM: ROCHE Amphi C
28-AM-Lunch 12h30 > 14h00 Déjeuner Libre & Exhibition (Poster / Stand) Pluriel Room
28-PM-Parallel-1 14h00 > 15h30 Myopathies Métaboliques Amphi A
  • Modérateur : P. Pascal LAFORET (Paris, France)
14h00 S18-01 > F. Federico MINGOZZI (Evry, France) 14h30 S18-02 > J. John VISSING (Copenhagen, Denmark) 15h00 S18-03 Thymidine Kinase 2 Deficiency: review of 16 Spanish patients with a late onset form > C. Carmen PARADAS (Antequera, Spain)
28-PM-Parallel-2 14h00 > 15h30 Thérapies Innovantes Amphi B
  • Modérateur : S. Shahram ATTARIAN (Marseille, France)
14h00 S19-01 A decoy trapping DUX4 for the treatment of FacioScapuloHumeral Muscular Dystrophy > J. Julie DUMONCEAUX (London, United Kingdom) 14h30 S19-02 CRISPR/Cas9 genome editing to generate new zebrafish models of centronuclear myopathy > E. Eléonore DUPUIS (Brussels, Belgium) 15h00 S19-03 TcDNA-ASO-mediated exon skipping approach for brain dystrophins restoration and compensation of cognitive/behavioral deficits in mouse models of DMD > F. Faouzi ZARROUKI (Montigny-Le-Bretonneux, France) 15h15 S19-04 Gene Therapy For Peripheral Neuropathy CMT1A > N. Nicolas TRICAUD (Montpellier, France)
28-PM-Coffee 15h30 > 16h00 Pause Café & Exhibition (Poster / Stand) Pluriel Room
28-PM-Surprise Box 16h00 > 17h00 Surprise Box Amphi A
  • Modérateur : B. Bertrand FONTAINE (Paris, France)
16h00 S20-01 16h15 S20-02 16h30 S20-03 16h45 S20-04
28-SPM-Closing 17h00 > 17h30 Cérémonie de Clôture Amphi A
17h00 S21-01

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