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AGELYSPARK

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Role of the lysosomal dysfunction during aging and implication for Parkinson s...

Role of the lysosomal dysfunction during aging and implication for Parkinson s Disease Parkinson’s disease (PD) is a chronic progressive neurodegenerative disorder with no proven neuroprotective or neurorestorative therapy. The most consistent risk factor for developing PD is increasing age. PD is a disease where su... ver más

02/12/2013

UBx

45K€

Presupuesto del proyecto: 45K€

Líder del proyecto

UNIVERSITE DE BORDEAUX No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

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Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2013-12-02 No tenemos la información de la convocatoria

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2 Participantes

UBx

0.00€ | Lider

UB2

N.D. | Participante

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Líder del proyecto

UNIVERSITE DE BORDEAUX No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 45K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Parkinson’s disease (PD) is a chronic progressive neurodegenerative disorder with no proven neuroprotective or neurorestorative therapy. The most consistent risk factor for developing PD is increasing age. PD is a disease where substantial cell loss in the substantia nigra pars compacta occurs alongside the formation of Lewy Bodies (LB). Although LB represent a pathological hallmark of PD, their mechanisms of formation and significance for the disease process remain unknown. In Specific Aim (SA) I, we will assess the role of the lysosomal dysfunction during aging and in PD, and its implication in the cell death and in the process of aggregate formation relevant to PD. This project will be tested (i) in vitro, using senescence accelerated cells, in physiological conditions, with pharmacological and genetic inhibition of the lysosomal-mediated degradation pathway, and with different PD-related cellular alterations (ii) in vivo, using senescence-accelerated mouse, to promote age-dependent aggregates formation following exposure with PD-related cellular alterations. In SA II, we will study the ill-defined protein ATP13A2 which the mutations are associated with Hereditary Parkinsonism. We will characterize (i) in vitro the functions in physiologic situation and we will analyse the consequences of the ATP13A2 mutated proteins in the lysosomal function and in cell death. We will assess the implication of this protein towards the accumulation of non-degraded material and also aggregates formation (ii) in vivo with the generation of a transgenic mouse for the mutation of ATP13A2 on the long view. In SA III, we hypothesize that the presence of a pathogenic factor in the brain milieu could affect the aggregate formation and/or the death of dopaminergic neurons. This hypothesis will be tested (i) in vivo, by injecting filtrated fractions coming from cerebrospinal fluid from PD patients in non-human primates brains and we will let those animals getting older for years.

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