EPIREGAD

Epigenetic regulation of Alzheimer's disease related genes

Coordinatore	UNIVERSITY OF LEEDS    more  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

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

 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.'