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REPLACES

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Restorative Plasticity At Corticostriatal Excitatory Synapses

Long-lasting, activity-dependent synaptic changes are thought to underlie the ability of the brain to translate experiences into memories and seem to represent the cellular model underlying learning and memory processes. Alteratio... ver más

30/04/2013

UMIL

5M€

Presupuesto del proyecto: 5M€

Líder del proyecto

UNIVERSITA DEGLI STUDI DI MILANO No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Ver 13 Participantes

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2013-04-30 No tenemos la información de la convocatoria

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Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

13 Participantes

UMIL

0.00€ | Lider

FONDAZIONE SANTA LUCIA

N.D. | Participante

CARDIFF UNIVERSITY

N.D. | Participante

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Líder del proyecto

UNIVERSITA DEGLI STUDI DI MILANO No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 5M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Long-lasting, activity-dependent synaptic changes are thought to underlie the ability of the brain to translate experiences into memories and seem to represent the cellular model underlying learning and memory processes. Alteration of brain plasticity may lead to the motor and cognitive disturbances observed in neurodegenerative diseases. Therapeutic approaches targeting synaptic plasticity could prevent neuronal degeneration and restore altered motor and cognitive functions. Long-term synaptic plasticity, long-term potentiation and long-term depression, are widely expressed at excitatory synapses throughout the brain and have both been described at corticostriatal connections, at which they might underlie motor-skill learning, cognitive performance and reward mechanisms. Unique feature of corticostriatal plasticity is the observation that the loss of these opposite forms of synaptic plasticity has been observed in experimental models of neurodegenerative disorders such as Parkinson’s disease (PD). REPLACES will use cortical striatal plasticity and its alterations in experimental PD to explore basic mechanisms of brain plasticity and repair and to translate the new generated knowledge into novel restorative therapeutic approaches. The long-term efficacy of new treatments for PD will be conditioned by their ability to restore, structurally and functionally, the synaptic wiring of striatal neurons and physiological synaptic plasticity. REPLACES addresses the potential restorative effects of either novel pharmacological treatments or neuronal transplants on the corticostriatal microcircuitry. Since chronic treatment with DA precursor L-DOPA induces in the majority of PD patients a maladaptative plasticity causing dyskinesia, innovative strategies should prevent the development of this disabling condition. REPLACES will characterize corticostriatal synaptic plasticity from molecular aspects to clinical neurophysiology involving behavioural and morphological analysis.

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