TRAFFICINAD

The role of neuronal intracellular traffic in Alzheimer´s disease

Coordinatore	FACULDADE DE CIENCIAS MEDICAS DA UNIVERSIDADE NOVA DE LISBOA    more  Organization address address: CAMPO MARTIRES DA PATRIA 130 city: LISBOA postcode: 1169 056 contact info Titolo: Mrs. Nome: Cristina Cognome: Fernandes Email: send email Telefono: +351 21 880 30 91 Fax: +351 21 880 30 87
Nazionalità Coordinatore	Portugal [PT]
Totale costo	100˙000 €
EC contributo	100˙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-2012-CIG
Funding Scheme	MC-CIG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-04-01   -   2017-03-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	FACULDADE DE CIENCIAS MEDICAS DA UNIVERSIDADE NOVA DE LISBOA  Organization address address: CAMPO MARTIRES DA PATRIA 130 city: LISBOA postcode: 1169 056 contact info Titolo: Mrs. Nome: Cristina Cognome: Fernandes Email: send email Telefono: +351 21 880 30 91 Fax: +351 21 880 30 87	PT (LISBOA)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'In neurons of Alzheimer’s disease (AD) there is an aberrant accumulation of beta-amyloid (Aβ) at synapses that renders difficult the formation of new memories for AD patients. Intracellular trafficking abnormalities have been implicated in Aβ accumulation. This research project aims to define how neuronal intracellular trafficking is mechanistically involved in Aβ accumulation that leads to AD. We will determine how the intracellular itinerary of the amyloid precursor protein in neurons influences the generation of Aβ. We will determine the intracellular trafficking of lysosomal hydrolases in neurons and their contribution to the lysosomal clearance of Aβ. Furthermore, we will investigate the mechanism whereby regulators of intracellular trafficking identified as risk-factors for AD contribute to Aβ accumulation. Finally, because aging is the most important risk factor for AD, we will determine if alterations in intracellular trafficking occur in aging, identifying a new mechanism of vulnerability to neurodegeneration in AD. Thus, we will demonstrate how intracellular trafficking is implicated in AD and unravel an important disease mechanism.'