AD PATHOGENESIS

Role of CRMP2 and Pin1 in the pathogenesis of Alzheimer’s disease

Coordinatore	USTAV MOLEKULARNI GENETIKY AKADEMIE VED CESKE REPUBLIKY VEREJNA VYZKUMNA INSTITUCE    more  Organization address address: VIDENSKA 1083 city: PRAHA 4 postcode: 142 20 contact info Titolo: Dr. Nome: Radislav Cognome: Sedlacek Email: send email Telefono: +420 2 41063198
Nazionalità Coordinatore	Czech Republic [CZ]
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)	2013-03-01   -   2017-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	USTAV MOLEKULARNI GENETIKY AKADEMIE VED CESKE REPUBLIKY VEREJNA VYZKUMNA INSTITUCE  Organization address address: VIDENSKA 1083 city: PRAHA 4 postcode: 142 20 contact info Titolo: Dr. Nome: Radislav Cognome: Sedlacek Email: send email Telefono: +420 2 41063198	CZ (PRAHA 4)	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Collapsin response mediator protein 2 (CRMP2) is essential for neural development and function. It promotes axon growth but upon its phosphorylation it mediates axon retraction. Deregulation of CRMP2 has been implicated in Alzheimer’s disease (AD) where CRMP2 was detected to form hyperphosphorylated aggregates within neurofibrillary tangles. The mechanisms that regulate formation of CRMP2 aggregates are so far largely unknown. We have recently found that one CDK5-phosphorylated CRMP2 isoform is specifically stabilized by Pin1 - a unique phospho-specific isomerase linked to AD, suggesting that deregulation of Pin1 could contribute to AD related CRMP2 pathology. In the present proposal we will study how various CRMP2 isoforms are involved in CRMP2 aggregate formation and how high levels of Amyloid-b peptide, CDK5, and Pin1 affect phosphorylation, stability or localization of CRMP2 isoforms in AD using mouse models. Funding of the proposal will bring a new insight into the role of Pin1 in AD-related CRMP2 pathology.'