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MEMOSAD

Financiado

Cerrado

Memory loss in Alzheimer disease underlying mechanisms and therapeutic targets

MEMOSAD aims at defining the molecular mechanisms of Abeta- and Tau-induced synaptotoxicity and at developing disease-modifying therapeutics for the prevention of memory loss in Alzheimer disease (AD). Insoluble aggregates of the... ver más

30/06/2011

VFBE

4M€

Presupuesto del proyecto: 4M€

Líder del proyecto

VERUM- STIFTUNG FUER VERHALTEN UND UMWELT No se ha especificado una descripción o un objeto social para esta compañía.

Fecha límite participación Sin fecha límite de participación.

Ver 9 Participantes

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2011-06-30 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.

9 Participantes

VFBE

333.50K€ | Lider

KU Leuven

200.40K€ | Participante

UDSL

420.00K€ | Participante

VLAAMS INSTITUUT BIOTECHNOL...

420.00K€ | Participante

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Líder del proyecto

VERUM- STIFTUNG FUER VERHALTEN UND UMWELT No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 4M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto MEMOSAD aims at defining the molecular mechanisms of Abeta- and Tau-induced synaptotoxicity and at developing disease-modifying therapeutics for the prevention of memory loss in Alzheimer disease (AD). Insoluble aggregates of the two proteins provide the pathological hallmarks of this incurable brain disorder. Early stage AD is characterized by a remarkably pure impairment of declarative memory and several lines of evidence suggest that this memory impairment is independent of the insoluble aggregates, does not require neuronal death and is caused by subtle and transient synaptic changes. The toxic Abeta and Tau species that cause synaptic dysfunction, their mechanism of toxicity and the link between both pathologies remain largely unknown, but recent data suggest that Abeta accumulation triggers Tau pathology. Consequently, primary neuronal cultures and animal models (C.elegans,zebrafish,mouse) will be employed to define the pathologic pathways leading from Abeta through Tau to synaptotoxicity. Initial experiments will investigate the effect of well-defined Abeta species on long term potentiation, synaptic morphology, gene expression, Tau phosphorylation/aggregation, axonal transport and behaviour. Similarly, we will investigate the functional consequences of Tau misfunction, aggregation, hyperphosphorylation and missorting in various cell culture systems (retinal ganglion cells, primary hippocampal neurons, organotypical slices) and animal models, especially with regard to intraneuronal trafficking and synaptic function. Once the toxic Abeta and Tau species are known and their mechanism of toxicity are defined, we will investigate how these pathways interact. Unravelling the pathologic pathways that lead from Abeta through Tau to synaptotoxicity and memory loss should reveal novel points for therapeutic intervention. Our aim is to deliver 3 or 4 validated therapeutic targets and at least 2 compounds with demonstrated therapeutic efficacy in mouse models of AD.

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