The interplay between oxidative stress and inflammation supports autistic-related behaviors in mice
Pangrazzi, L.; Cerilli, E.; Balasco, L.; Tobia, C.; Dall'O', G. M.; Chelini, G.; Perini, S.; Filosi, M.; Ravizza, T.; Vezzani, A.; Provenzano, G.; Pastore, A.; Weinberger, B.; Domenici, E.; Bozzi, Y.
Show abstract
Autism Spectrum Disorder (ASD) is a highly prevalent neurodevelopmental condition characterized by social communication deficits and repetitive/restricted behaviors. Several studies showed that inflammation may contribute to ASD. Here we used RT-qPCR, RNA sequencing, immunohistochemistry, and flow cytometry to show that pro-inflammatory molecules were increased in the cerebellum and periphery of mice lacking Cntnap2 (Cntnap2-/-), a robust model of ASD. In parallel, oxidative stress was present in the cerebellum of mutant animals. Systemic treatment with N-acetyl-cysteine (NAC) rescued cerebellar oxidative stress and inflammation as well as motor and social impairments in Cntnap2-/- mice. This was accompanied by improved function of microglia cells in NAC-treated mutant animals. Intriguingly, social deficits, cerebellar inflammation and microglia dysfunction were induced by NAC in Cntnap2+/+animals. Our findings therefore suggest that the interplay between oxidative stress and inflammation may support ASD-related behaviors in mice.
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