EPIREGAD

Epigenetic regulation of Alzheimer's disease related genes

 Coordinatore UNIVERSITY OF LEEDS 

 Organization address address: WOODHOUSE LANE
city: LEEDS
postcode: LS2 9JT

contact info
Titolo: Mr.
Nome: Martin
Cognome: Hamilton
Email: send email
Telefono: +44 113 343 4090
Fax: +44 113 343 4090

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 101˙274 €
 EC contributo 101˙274 €
 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-2010-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-10-01   -   2012-09-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY OF LEEDS

 Organization address address: WOODHOUSE LANE
city: LEEDS
postcode: LS2 9JT

contact info
Titolo: Mr.
Nome: Martin
Cognome: Hamilton
Email: send email
Telefono: +44 113 343 4090
Fax: +44 113 343 4090

UK (LEEDS) coordinator 101˙274.80

Mappa


 Word cloud

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trafficking    protein    beta    metabolites    nuclear    nep    disease    amyloid    aicd    gene    abeta    ad    neuronal    genes    chromatin    regulation    app   

 Obiettivo del progetto (Objective)

'Alzheimer’s disease (AD) and other dementias affect over 7 million individuals in Europe. There is, as yet, no treatment to halt or reverse disease progression despite huge investments into research. The accumulation of the amyloid beta-peptide (Abeta), derived from the amyloid precursor protein (APP) in the brain, is a key factor in the development of AD but the roles of other APP metabolites are poorly understood. This project will focus on one of these metabolites, its intracellular domain, AICD, and the mechanism for its nuclear trafficking and gene transcriptional regulation, especially of the Abeta-degrading enzyme, neprilysin (NEP), which maintains Abeta homeostasis. These studies will focus on the differential contributions of the three APP isoforms to AICD production, nuclear trafficking and gene regulation, and will use a variety of neuronal and non-neuronal models to analyse epigenetic changes mediating NEP expression including chromatin composition of the NEP gene in active and downregulated states and whether APP isoform effects are direct or indirect. In parallel, other putative AICD-responsive genes will be compared (aquaporin, GSK-3beta). This will allow us to formulate strategies for up-regulation of key neuroprotective genes in disease leading to potential new therapeutic approaches. The project will provide the Research Fellow with broad experience in molecular neuroscience (from bioimaging and protein trafficking to chromatin analysis and gene regulation) in a well-founded, integrated and multi-disciplinary environment for AD research.'

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