MECPST-IPDProject reference: 331924
Funded under :
Identification of inflammation pathways involved in the predisposition to decreased neurogenesis and depression
Total cost:EUR 221 606,4
EU contribution:EUR 221 606,4
Coordinated in:United Kingdom
Topic(s):FP7-PEOPLE-2012-IEF - Marie-Curie Action: "Intra-European fellowships for career development"
Call for proposal:FP7-PEOPLE-2012-IEFSee other projects for this call
Funding scheme:MC-IEF - Intra-European Fellowships (IEF)
"Current drug therapies for depression have clinical benefits for many patients, however, there remains a large number of patients who either do not become entirely enabled or do not have any clinical benefits whatsoever. Depression is estimated to cost society financially upward of 1% GDP, not to mention the toll on those suffering from depression including their families. During the past decades, enormous resources have been spent to find new mechanisms through which to treat the disease though without any results thus forcing researchers to change strategy. One development has been the general acceptance that depression may be composed of several pathologies rather than a single disease mechanism. In this project we incorporate three potential pathologies which have recently been associated with depression. The first is stress which is known as a common cause of depression followed by adult neurogenesis which has recently been suggested to regulate stress. Finally, inflammation has most recently been suggested to develop into a pathology which can cause depression. Our latest research has shown specifically an association between depressed individuals who are exposed to early life stress and inflammation and furthermore that these exposed individuals have an increased level of inflammation even in the absence of depression. We have therefore developed a hypothesis that individuals exposed to early life stress have an inflammatory predisposition and have a larger chance of developing depression if other pathologies (stress/decreased neurogenesis) are also present. If this hypothesis is validated, treatment methods targeting this predisposition will be of significant interest. To test this hypothesis we plan to develop an animal model which incorporates these pathologies which we can then further use to discover and thereafter test new treatment targets."
EU contribution: EUR 221 606,4
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