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The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

ABSTRACT: The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

PROVIDER: PRJNA1110187 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28995700_1.fastq.gz	Fastqsanger.gz
	SRR28995700_2.fastq.gz	Fastqsanger.gz
	SRR28995701_1.fastq.gz	Fastqsanger.gz
	SRR28995701_2.fastq.gz	Fastqsanger.gz
	SRR28995702_1.fastq.gz	Fastqsanger.gz

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The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

Project description: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 lackingCntnap2(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 inCntnap2-/-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 inCntnap2+/+animals. Our findings therefore suggest that the interplay between oxidative stress and inflammation may support ASD-related behaviors in mice.

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