Identification and modulation of pathogenic Amyloid beta-peptide species


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 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


# participant  country  role  EC contrib. [€] 

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
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

 Organization address address: GESCHWISTER SCHOLL PLATZ 1
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


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

proteins    pathway    search    species    imaging    modifiers    secretase    binding    generation    szlig    neurotoxicity    amyloid    ad    cascade    pathology    rna    disease    spreading    initiate   

 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.'

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