IGF-I GENE THERAPY PREVENTS GLIA ACTIVATION AFTER A STAB WOUND INJURY IN THE BRAIN.

BELLINI MJ; BANDÍN-CARAZO S; AZCOITIA I; GARCIA-SEGURA LM

Oviedo

Congreso; XV Congreso Nacional de la Sociedad Española de Neurociencia SENC; 2013

Sociedad Española de Neurociencias

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity worldwide. Despite extensive efforts to develop neuroprotective therapies for this devastating disorder there have been no successful outcomes in human clinical trials to date. Neuroinflammation is well established as a key secondary injury mechanism after TBI, and it has been long considered to contribute to the damage sustained following brain injury. It comprises a feature of many neurological disorders that is accompanied by the activation of glial cells and the release of pro-inflammatory cytokines and chemokines. Such activation is a normal response oriented to protect neural tissue and it is mainly regulated by microglia and astroglia. However, excessive and chronic activation of glia may lead to neurotoxicity and may be harmful for neural tissue. The role of glia in this process has been well recognized and they have been regarded as promising targets for development of anti-inflammatory therapies. Neurotrophic factors are small molecules that exert different functions in the central nervous system (CNS), among them insulin-like growth factor-I (IGF-I) exerts neuroprotective actions that are mediated at least in part by control of activation of glia. In this study we have assessed the efficacy of IGF-I gene therapy in reducing the inflammatory response of astrocytes and microglia after a stab wound injury.