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Dr Riccardo Brambilla 


Riccardo Brambilla is a leading figure in the emerging field of Molecular and Cellular Cognition. Council Member of the Molecular and Cellular Cognition Society (MCCS; www.molcellcog.org) he is also Founding President of the sister organisation European Molecular and Cellular Cognition Society (EMCCS; http://emccs.haifa.ac.il/), since 2008 part of the Federation of European Neuroscience Societies (FENS).

He has been working in the field of signal transduction since 1987 and in molecular neuroscience since 1993, being post-doctoral fellow in the laboratory of Ruediger Klein at the European Molecular Biology Laboratory. In Heidelberg he learned mouse genetics techniques such as gene targeting and successfully applied them to the neurobiology of learning and memory. In particular he generated the Ras-GRF1 KO mouse strain that was the first published genetic model demonstrating a direct involvement of the Ras-ERK-CREB signalling cascade in behavioural plasticity (Brambilla et al, Nature, 1997, cited so far 321times). 

During the last 16 years as a group leader Dr. Brambilla has continued to work 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 recently implicated in certain forms of autism, results in procedural learning improvements and in increased synaptic plasticity in the striatum (Mazzucchelli et al, 2002, Neuron, cited so far 247 times). This phenotype is likely to be due to an abnormal hyperactivation of the remaining ERK2 isoform, suggesting a potential mechanism for some autism spectrum disorders associated to deregulated cell signalling in the brain. In more recent years, Dr. Brambilla 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 (Fasano et al, 2009, Biol Psych; Fasano et al, 2010, PNAS, Cerovic et al, 2013, in press). Over the years his laboratory has developed new molecular biology tools to modulate gene expression in the brain via lentiviral vectors and cell permeable peptides (CPP). In particular, he recently patented CPPs able to either block or potentiate Ras-ERK signalling in the brain and he will try to develop them into clinically relevant therapeutics for several neuropsychiatric disorders: Parkinson’s Disease (PD) and related disorders, including L-DOPA induced Dyskinesia (LID); Huntington’s Disease (HD); Mental Retardation Syndromes and Autism Spectrum Disorders (ASD) and drug addiction.