Explore the words cloud of the ALS-Networks project. It provides you a very rough idea of what is the project "ALS-Networks" about.
The following table provides information about the project.
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE
|Coordinator Country||France [FR]|
|Total cost||2˙000˙000 €|
|EC max contribution||2˙000˙000 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2017-04-01 to 2022-03-31|
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|1||INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE||FR (PARIS)||coordinator||2˙000˙000.00|
Brain and spinal cord diseases affect 38% of the European population and cost over 800 billion € annually; representing by far the largest health challenge. ALS is a prevalent neurological disease caused by motor neuron death with an invariably fatal outcome. I contributed to ALS research with the groundbreaking discovery of TDP-43 mutations, functionally characterized these mutations in the first vertebrate model and demonstrated a genetic interaction with another major ALS gene FUS. Emerging evidence indicates that four major causative factors in ALS, C9orf72, TDP-43, FUS & SQSTM1, genetically interact and could function in common cellular mechanisms. Here, I will develop zebrafish transgenic lines for all four genes, using state of the art genomic editing tools to combine simultaneous gene knockout and expression of the mutant alleles. Using these innovative disease models I will study the functional interactions amongst these four genes and their converging effect on key ALS pathogenic mechanisms: autophagy degradation, stress granule formation and RNA regulation. These studies will permit to pinpoint the molecular cascades that underlie ALS-related neurodegeneration. We will further expand the current ALS network by proposing and validating novel genetic interactors, which will be further screened for disease-causing variants and as pathological markers in patient samples. The power of zebrafish as a vertebrate model amenable to high-content phenotype-based screens will enable discovery of bioactive compounds that are neuroprotective in multiple animal models of disease. This project will increase the fundamental understanding of the relevance of C9orf72, TDP-43, FUS and SQSTM1 by developing animal models to characterize common pathophysiological mechanisms. Furthermore, I will uncover novel genetic, disease-related and pharmacological modifiers to extend the ALS network that will facilitate development of therapeutic strategies for neurodegenerative disorders
|year||authors and title||journal||last update|
Hortense de Calbiac, Adriana Dabacan, Elise Marsan, HervÃ© Tostivint, Gabrielle Devienne, Saeko Ishida, Eric Leguern, StÃ©phanie Baulac, Raul C. Muresan, Edor Kabashi, Sorana Ciura
Depdc5 knockdown causes mTOR-dependent motor hyperactivity in zebrafish
published pages: 510-523, ISSN: 2328-9503, DOI: 10.1002/acn3.542
|Annals of Clinical and Translational Neurology 5/5||2019-05-14|
Shunmoogum A. Patten, Dina Aggad, Jose Martinez, Elsa Tremblay, Janet Petrillo, Gary A.B. Armstrong, Alexandre La Fontaine, Claudia Maios, Meijiang Liao, Sorana Ciura, Xiao-Yan Wen, Victor Rafuse, Justin Ichida, Lorne Zinman, Jean-Pierre Julien, Edor Kabashi, Richard Robitaille, Lawrence Korngut, J. Alexander Parker, Pierre Drapeau
Neuroleptics as therapeutic compounds stabilizing neuromuscular transmission in amyotrophic lateral sclerosis
published pages: , ISSN: 2379-3708, DOI: 10.1172/jci.insight.97152
|JCI Insight 2/22||2019-05-14|
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