Increasing evidence supports the" inflammatory hypothesis in AD" according to which neuronal damages in this age-related disease are caused not only by the fundamental pathology but also by the local inflammatory response to it sustained by reactive glib. Recent findings demonstrate a sophisticated integration between neurons and atrocities. Inflammatory atrocities undergo morph functional changes, which may perturb neuron-atrocity interaction and result in neuronal sufferance. By identifying and targeting harmful pathways in inflammatory atrocities we will define potential new therapeutic approaches to prevent or delay AD progression. This consortium combines complementary expertise to: a) assess the "inflammatory hypothesis of AD" and the role of atrocities in transgenic models; b) identify targets of inflammation-neurodegeneration coupling in atrocities; c) validate drug strategies against them; d) test these therapeutically strategies in AD transgenic.
Funding SchemeCSC - Cost-sharing contracts
16672 Glyfada (Attiki)
RG21 6XA Basingstoke