MICROGLIA AND AMD
Subretinal Microglia accumulation play a decisive role in the development of Age-related Macular Degeneration
| Coordinatore | INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | France [FR] |
| Totale costo | 1˙560˙000 € |
| EC contributo | 1˙560˙000 € |
| 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-2007-StG |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2008 |
| Periodo (anno-mese-giorno) | 2008-09-01 - 2013-08-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)
Organization address
address: 101 Rue de Tolbiac contact info |
FR (PARIS) | hostInstitution | 0.00 |
| 2 |
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)
Organization address
address: 101 Rue de Tolbiac contact info |
FR (PARIS) | hostInstitution | 0.00 |
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Obiettivo del progetto (Objective)
'Age-related macular degeneration (AMD) is the leading cause of vision loss in the Europe. New anti-angiogenic therapies of AMD do not treat the neurodegenerative aspect of AMD. Recent evidence suggests an implication of inflammatory mediators in AMD. We have focused our interest on the potential role of chemokines (Ch) and microglial cells (MC) in this condition. Our data concerning the chemokine receptor (CR) CX3CR1, indicates that (i) CR are expressed on MCs in human and mice; (ii) CR-positive MC accumulate in affected areas of the macula in human AMD, (iii) CX3CR1 deficient mice develop age dependent subretinal MC accumulation, Drusen formation, retinal degeneration and exacerbated neovascularization, similarly to AMD. Our data suggests an important role of subretinal MC accumulation in the development of AMD. We hypothesize that (1) function altering polymorphisms in genes of Ch pathways are associated with AMD, that (2) this pathway dysfunction leads to MC accumulate in the subretinal space with age and (3) the consequential prolonged MC presence in the subretinal space leads to cardinal features of AMD (Drusen, retinal degeneration, neovascularization). Therefore we believe that decreasing subretinal MCs or interfering with their neurotoxic and angiogenic factors will inhibit AMD development. Our specific aim is to study (1) polymorphisms of Ch pathways in AMD and controls, (2) determine the Ch pathways involved in the recruitment and accumulation of MCs to the subretinal space, (3) determine the implication of MC in Drusen formation, retinal degeneration and neovascularization and characterize the implicated molecular mediators and (4) test the identified mediators of microglial cell neurotoxicity and angiogenicity as drug targets in AMD models. The aim of this work, from clinical polymorphism studies to transgenic mouse models, is to propose new mechanisms in the pathogenesis of AMD and to develop novel therapeutic strategies for the treatment of AMD.'