MECPST-IPD

Identification of inflammation pathways involved in the predisposition to decreased neurogenesis and depression

 Coordinatore KING'S COLLEGE LONDON 

 Organization address address: Strand
city: LONDON
postcode: WC2R 2LS

contact info
Titolo: Mr.
Nome: Paul
Cognome: Labbett
Email: send email
Telefono: +4420 7848 8184
Fax: 442078000000

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 221˙606 €
 EC contributo 221˙606 €
 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-2012-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-05-01   -   2015-04-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON

 Organization address address: Strand
city: LONDON
postcode: WC2R 2LS

contact info
Titolo: Mr.
Nome: Paul
Cognome: Labbett
Email: send email
Telefono: +4420 7848 8184
Fax: 442078000000

UK (LONDON) coordinator 221˙606.40

Mappa


 Word cloud

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

life    predisposition    benefits    stress    treatment    recently    suggested    pathologies    patients    clinical    inflammation    exposed    disease    individuals    neurogenesis    hypothesis    depression   

 Obiettivo del progetto (Objective)

'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.'

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