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Séminaire

Towards Novel Therapeutics for Cognitive Deficits Associated to RASopathies and Autism Spectrum Disorder

Pr Riccardo BRAMBILLA
Cardiff University, Neuroscience Division, School of Biosciences, Royaume-Uni

mardi 06 février 2018 - 11h00 - Auditorium, IGBMC
Invité(e) par Médecine translationnelle et neurogénétique, Yann HERAULT

Professor Brambilla is a leading figure in the emerging field of Molecular and Cellular Cognition. Over the last several decades, he has worked on the role of synaptic signalling in behavioural plasticity and demonstrated that ERK1 and Ras-GRF1 are essential for normal and abnormal behavioural plasticity in the striatum. In his seminal paper in 2002, he demonstrated that loss of ERK1 MAP kinase, a gene implicated in certain forms of autism, results in procedural learning improvements and increased synaptic plasticity in the striatum. In recent years, he has published important works on the role of Ras-GRF1, a synaptic integrator of Ras-ERK signalling the basal ganglia, in pathological processes such as drug addiction and L-DOPA induced Dyskinesia, a severe motor complication of Parkinson’s DIsease. His laboratory has developed new molecular biology tools to modulate therapeutically gene expression in the brain and is actively pursuing repositioning of clinically relevant drugs. In this seminar, he will present his recent findings on mechanisms underlying cognitive impairments associated with certain forms of RASopathies and Autism Spectrum Disorder, providing an intellectual framework for future therapeutic approaches in translational neuroscience that may apply to a broader range of brain disorders.

Professor Brambilla is a leading figure in the emerging field of Molecular and Cellular Cognition. Over the last several decades, he has worked on the role of synaptic signalling in behavioural plasticity and demonstrated that ERK1 and Ras-GRF1 are essential for normal and abnormal behavioural plasticity in the striatum. In his seminal paper in 2002, he demonstrated that loss of ERK1 MAP kinase, a gene implicated in certain forms of autism, results in procedural learning improvements and increased synaptic plasticity in the striatum. In recent years, he has published important works on the role of Ras-GRF1, a synaptic integrator of Ras-ERK signalling the basal ganglia, in pathological processes such as drug addiction and L-DOPA induced Dyskinesia, a severe motor complication of Parkinson’s DIsease. His laboratory has developed new molecular biology tools to modulate therapeutically gene expression in the brain and is actively pursuing repositioning of clinically relevant drugs. In this seminar, he will present his recent findings on mechanisms underlying cognitive impairments associated with certain forms of RASopathies and Autism Spectrum Disorder, providing an intellectual framework for future therapeutic approaches in translational neuroscience that may apply to a broader range of brain disorders.

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