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Agency: Cordis | Branch: FP7 | Program: MC-ITN | Phase: FP7-PEOPLE-ITN-2008 | Award Amount: 5.06M | Year: 2009

SyMBaD aims to move forward our knowledge on synapse structure and function in the normal and pathological brain. Brain diseases represent a considerable social and economic burden in Europe. Emerging evidence indicates that synaptic dysfunction is associated with a majority of neurological and psychiatric disorders. Novel therapeutical approaches relie on a better knowledge of the synapse and its pathologies. The network comprises 23 teams from 6 academic centres (Bordeaux, Alicante, Milan, Geneva, Gttingen, Bristol) representing an important fraction of the leading European researchers in the field. Synergies and complementarities between the research teams exist and should develop with the activities of the SyMBaD network. The participants are already well integrated in European scientific collaborative networks, and have an outstanding track-record of training young researchers. Industrial partners (6) will take part as full partners in training by an obligatory placement from 6 to 12 months of 16 ESR among the 26 recruited. The other ESR will be fully integrated into collaborative projects between academic teams. The private sector comprises companies involved in the development of new therapeutical strategies to combat brain diseases (GSK, Neurosearch, Xygen, and Noscira) and companies involved in technical development to be used in synaptic research and beyond (Bioxtal, Amplitude Systems, Explora Nova). The SYMBAD network aims to: Teach a number of increasingly sophisticated techniques required in neuroscience and to advance towards novel therapies. Focus on technological innovation and on interweaving of multilevel approaches. Facilitate future constructive dialogue between academia and industry in the field by involving SMEs in the training of PhD students through collaborative research projects. SyMBaD will make European Neuroscience more attractive to young scientists, it will catalyze multi-level collaborations and foster intersectorial exchanges to advance in the study of some of the foremost Health issues of the European Community.

Agency: Cordis | Branch: FP7 | Program: CP-FP | Phase: HEALTH-2007-2.2.1-7 | Award Amount: 5.08M | Year: 2008

Neuronal circuits in mammalian brain act predominantly via excitatory synapses on dendritic spines. Formation of new spines in adult brain constitutes the structural basis of neuronal plasticity. The underlying molecular mechanisms remain largely unknown but depend essentially on kinase-dependent signalling pathways. Final formation of synapses on spines depends on dynamic interactions of microtubuli and actin-filaments that are also controlled by kinases. Deterioration of these processes to different extents are thought to cause the cognitive decline in normal ageing as well in Alzheimers disease (AD) and familial fronto-temporal dementia (FTD). Protein tau is a microtubule associated protein and GSK-3 kinases are proposed as the major tau-kinases in vivo. Their exact contributions remain to be functionally defined in vivo both in normal neuronal plasticity and in degeneration. We develop pre-clinical models for AD and FTD that have tauopathy in common as essential pathogenic component and will explore the GSK-3 kinases in vivo by manipulating their activity genetically, pharmacologically and biochemically. Inhibitors are wanted that are effective and specific and enter brain in vivo. This proposal engages in three activities: (i) elucidate physiological functions of GSK-3 kinases in synaptic plasticity in adult and ageing brain, and in degenerating brain; define fundamental neuron-specific functions of GSK-3 kinases in vivo in novel mouse models; define contributions of GSK-3 kinases to amyloid and to tau pathology, separately and combined in vivo in validated mouse models (ii) design novel inhibitors of GSK-3 kinases and alternative tools to inhibit GSK-3 activity in vivo (iii) test pharmacological and peptidometic inhibitors of GSK-3 in validated mouse models of neurodegeneration for their restorative potential; analyse their mode of action and their acute and chronic effects by multi-parametric analysis

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