NOGORISE

The Nogo-A receptor complex after CNS injury and its role in the developing and adult nervous system

Coordinatore	UNIVERSITAET ZUERICH    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Switzerland [CH]
Totale costo	2˙500˙000 €
EC contributo	2˙500˙000 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2011-ADG_20110310
Funding Scheme	ERC-AG
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-06-01   -   2017-05-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITAET ZUERICH  Organization address address: Raemistrasse 71 city: ZURICH postcode: 8006 contact info Titolo: Prof. Nome: Martin Cognome: Schwab Email: send email Telefono: +41 44 6353266 Fax: +41 44 6353303	CH (ZURICH)	hostInstitution	2˙500˙000.00
2	UNIVERSITAET ZUERICH  Organization address address: Raemistrasse 71 city: ZURICH postcode: 8006 contact info Titolo: Prof. Nome: Martin Ernst Cognome: Schwab Email: send email Telefono: +41 44 635 33 30 Fax: +41 44 635 33 03	CH (ZURICH)	hostInstitution	2˙500˙000.00

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 Obiettivo del progetto (Objective)

'Repulsive guidance cues for growing axons and factors inhibiting neurite growth are increasingly recognized as key players for nerve fiber growth and plasticity in the developing and adult nervous system. The first neurite growth inhibitory factor discovered in the context of axonal regeneration in the adult central nervous system (CNS) was the membrane protein Nogo-A. Inactivation of Nogo-A, e.g. by neutralizing antibodies, after spinal cord injury, brain injury or stroke leads to improved functional recovery in parallel with long distance regeneration of injured fibers and enhanced compensatory sprouting. The molecular mechanisms of action of Nogo-A is only partially known; a key element, the Nogo-A-specific receptor has remained undefined. We have recently found a membrane protein that binds to Nogo-A with high affinity; blockers of this new receptor neutralize many of the typical Nogo-A effects in vitro. The present proposal addresses new aspects of the mechanism of action and the in vivo roles of this novel Nogo-A receptor and its interactions with the known Nogo receptor components. The new results will contribute to the molecular and physiological understanding of Nogo-A and related growth inhibitors in the nervous system. Together with the currently ongoing clinical trial to enhance recovery after spinal cord injury in patients by anti-Nogo-A antibodies, the results of the present project will form an important basis for further treatments in brain injury and stroke.'