GXE-MOLMECH
Gene x environment interactions in affective disorders - elucidating molecular mechanisms
| Coordinatore | MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Germany [DE] |
| Totale costo | 1˙254˙119 € |
| EC contributo | 1˙254˙119 € |
| 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-2011-StG_20101109 |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2012 |
| Periodo (anno-mese-giorno) | 2012-03-01 - 2017-02-28 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
Organization address
address: Hofgartenstrasse 8 contact info |
DE (MUENCHEN) | hostInstitution | 1˙254˙119.60 |
| 2 |
MAX PLANCK GESELLSCHAFT ZUR FOERDERUNG DER WISSENSCHAFTEN E.V.
Organization address
address: Hofgartenstrasse 8 contact info |
DE (MUENCHEN) | hostInstitution | 1˙254˙119.60 |
Mappa
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Obiettivo del progetto (Objective)
'Exposure to traumatic experiences as well as chronic stress has been shown to increase the risk for a number of psychiatric disorders including major depression and anxiety disorders by inducing longterm alterations in the reactivity of the stress hormone system. These effects can be moderated by genetic variants, one of them being functional polymorphisms in glucocorticoid receptor (GR) co-chaperone gene FKBP5. Preliminary studies in my laboratory suggest that this GxE interaction is mediated by allele-specific de-methylation of intronic glucocorticoid response elements (GREs) within FKBP5. The overarching aim of this grant is to identify the molecular mechanisms by which FKBP5 polymorphisms and early trauma interact to increase the risk for a number of depressive and anxiety disorders. In this application, I propose to extend these preliminary data by experiments in healthy controls and depressed patients, human lymphoblastiod cell lines as well as an animal model in outbred mice showing similar GxE interaction to address the molecular mechanism of these DNA-methylation changes as well as their cellular and system level consequences. Finally we will use expression quantitative trait locus analysis for GR stimulated gene expression to identify new loci relevant for GxE interactions in stress-related disorders. Overall, this proposal will follow up on one of the first putative molecular and systemic mechanisms identified for gene x environment interactions in affective disorders and will establish an animal model mimicking these specific interactions. The findings related to this proposal could be of major importance for understanding the biology of these disorders and to explore novel treatment options, including manipulations of epigenetic modifications.'