AMYLOID

Identification and modulation of pathogenic Amyloid beta-peptide species

Coordinatore	LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	2˙497˙020 €
EC contributo	2˙497˙020 €
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-2012-ADG_20120314
Funding Scheme	ERC-AG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-03-01   -   2018-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN  Organization address address: GESCHWISTER SCHOLL PLATZ 1 city: MUENCHEN postcode: 80539 contact info Titolo: Ms. Nome: Dorothee Cognome: Hasebrink Email: send email Telefono: +49 89 2180 3605 Fax: +49 89 2180 2985	DE (MUENCHEN)	hostInstitution	2˙497˙020.00
2	LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN  Organization address address: GESCHWISTER SCHOLL PLATZ 1 city: MUENCHEN postcode: 80539 contact info Titolo: Prof. Nome: Christian Cognome: Haass Email: send email Telefono: +49 89 2180 75471 Fax: +49 89 2180 75415	DE (MUENCHEN)	hostInstitution	2˙497˙020.00

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 Obiettivo del progetto (Objective)

'The frequency of Alzheimer's disease (AD) will dramatically increase in the ageing western society during the next decades. Currently, about 18 million people suffer worldwide from AD. Since no cure is available, this devastating disorder represents one of the most challenging socio-economical problems of our future. As onset and progression of AD is triggered by the amyloid cascade, I will put particular attention on amyloid ß-peptide (Aß). The reason for this approach is, that even though 20 years ago the Aß generating processing pathway was identified (Haass et al., Nature 1992a & b), the identity of the Aß species, which initiate the deadly cascade is still unknown. I will first tackle this challenge by investigating if a novel and so far completely overlooked proteolytic processing pathway is involved in the generation of Aß species capable to initiate spreading of pathology and neurotoxicity. I will then search for modulating proteins, which could affect generation of pathological Aß species. This includes a genome-wide screen for modifiers of gamma-secretase, one of the proteases involved in Aß generation as well as a targeted search for RNA binding proteins capable to posttranscriptionally regulate beta- and alpha-secretase. In a disease-crossing approach, RNA binding proteins, which were recently found not only to be deposited in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis but also in many AD cases, will be investigated for their potential to modulate Aß aggregation and AD pathology. Modifiers and novel antibodies specifically recognizing neurotoxic Aß assemblies will be validated for their potential not only to prevent amyloid plaque formation, but also spreading of pathology as well as neurotoxicity. In vivo validations include studies in innovative zebrafish models, which allow life imaging of neuronal cell death, as well as the establishment of microPET amyloid imaging for longitudinal studies in individual animals.'