AGELYSPARK

"Role of the lysosomal dysfunction during aging, and implication for Parkinson’s Disease."

Coordinatore	UNIVERSITE DE BORDEAUX    more  Organization address address: PLACE PEY BERLAND 35 city: BORDEAUX postcode: 33000 contact info Titolo: Mrs. Nome: Adeline Cognome: Barre Email: send email Telefono: 33557574678 Fax: 33557571557
Nazionalità Coordinatore	France [FR]
Totale costo	45˙000 €
EC contributo	45˙000 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2009-RG
Funding Scheme	MC-ERG
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-12-03   -   2013-12-02

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE DE BORDEAUX  Organization address address: PLACE PEY BERLAND 35 city: BORDEAUX postcode: 33000 contact info Titolo: Mrs. Nome: Adeline Cognome: Barre Email: send email Telefono: 33557574678 Fax: 33557571557	FR (BORDEAUX)	coordinator	45˙000.00
2	UNIVERSITE VICTOR SEGALEN BORDEAUX II  Organization address address: RUE LEO SAIGNAT 146 city: BORDEAUX CEDEX postcode: 33076 contact info Titolo: Dr. Nome: Erwan Cognome: Bezard Email: send email Telefono: +33 5 57 57 16 87 Fax: +33 5 56 98 61 82	FR (BORDEAUX CEDEX)	participant	0.00

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 Obiettivo del progetto (Objective)

'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.'