GLIA Edinburgh 2017: Abstracts Oral Presentation, Posters, Indexes

ÀNASETTI-NELLI, SOLEDAD; DOLCETTI, FRANCO JC; BELLINI, MJ; FALOMIR-LOCKHART, EUGENIA; HEREÑU, CB

GLIA

WILEY-LISS, DIV JOHN WILEY & SONS INC

Año: 2017 vol. 65 p. 90 - 91

0894-1491

The increase in average life expectancy is accompanied by an increment in the incidence of degenerative diseases associated with age. Aging adversely affects inflammatory processes in the brain, which has important implications in the context of disease progression. Many studies have demonstrated that neuroinflammation mediated by microglia and astroglia plays a key role in neuronal survival as well as in death. Furthermore, it has been proposed that microglia become dysfunctional with age and may lose their neuroprotective properties, leading to chronic neurodegeneration. Therefore, an adequate regulation of neuroinflammation is essential to prevent the progression of neurodegenerative diseases.A possible approach to control neuroinflammation is the use of neurotrophic factors. Among this, IGF-1 is well known by its neuroprotective role in the CNS. Moreover, our group has previously described that ICV IGF-1 gene therapy induced a significant improvement in motor performance in aged rats. Regarding this, we propose that restorative effects of IGF-1 in motor skills could be mediated by glial cells.In this work, we implemented ICV IGF-1 neuroprotective gene therapy in two models associated with motor impairment: the senile rat (28 month-old) and a rat model of Parkinson?s disease induced by nigral injection of LPS in young rats. We assessed the rat?s motor performance and analyzed the number, morphology and reactivity of glial cells.Results: ICV IGF-1 treatment recovered motor impairment in both animal models. Regarding the aging model, we observed a significant increase in the microglial cells number in IGF-1 treated rats, accompanied by a significant increment in their reactivity, presenting a higher percentage of M2 phenotype number. With respect to astrocytes, though we did not observed a significant difference in the cell number, experimental rats showed a more complex phenotype. Overall, we conclude that IGF1 ameliorates the motor impairment observed in both models, and that improvement could be due in part to the regulation of microglia activation.