Degree: Medical Degree (1991), University of Valencia. Ph.D program: PhD (1995). Department of Biochemistry and Molecular Biology, School of Medicine, University of Valencia. Posdoctoral Positions: Department of Molecular Genetics. Instituto de Investigaciones Citológicas (FVIB),Valencia (1996-99). Previous positions: Researcher. IBMC University Miguel Hernández (2000-02) Miguel Servet Researcher (2002-8) Instituto de Neurociencias UMH-CSIC and Hospital de San Juan (Alicante) Visiting Scientist: Zentrum Molekulare Neurobiologie Hamburg, Germany (2002) Department Pharmacology, University of Virginia USA (2003) Wolfson Institute for Biomedical Research, UCL, London UK (2005) Departmentt Pharmacology, University of Cambridge, UK, (2008) Wolfson Institute for Biomedical Research, London, UK (2010) Current Position: Group Leader Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO); Hospital General Universitario de Alicante and Instituto de Neurociencias UMH-CSIC

Research Fields: Human brain activity depends on the adequate communication between different neuronal networks that integrate the information from sensory organs and generate a coordinated response. Coordination is only possible thanks to the rapid nerve conduction velocity developed by vertebrates. For that, glial cells synthesize a highly specialized membrane (the myelin) that wrap and electrically insulate axons, allowing “saltatory conduction”. Our main goal is to understand how myelin is synthesized in health and how is lost in demyelianting diseases. Thanks to a complex bidirectional axon-glia communication system ensheathing glial cells (oligodendrocytes and Schwann cells) match exactly the number and length of neuronal axons. Glial cells also produce signalling molecules that heavily influence the axon integrity and growth. We are trying to understand which are the molecules that are produced by the axons to instruct glial cells towards myelination capability. We’ll use this information to try to avoid demyleination and/or improve re-myelination in different demyelinating diseases. We also try to find the glial produced signalling molecules and signalling pathways that modulate axon survival and growth. These activities could be useful not only to improve the treatment of demyelinating diseases but also to improve nerve regeneration after injury.