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ABSTRACT: Rat model of autism

PROVIDER: PRJNA616070 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11443149_1.fastq.gz	Fastqsanger.gz
	SRR11443149_2.fastq.gz	Fastqsanger.gz
	SRR11443150_1.fastq.gz	Fastqsanger.gz
	SRR11443150_2.fastq.gz	Fastqsanger.gz
	SRR11443151_1.fastq.gz	Fastqsanger.gz

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Project description:Maternal autoantibody related autism (MARA), in which mothers produce specific patterns of autoantibodies during pregnancy, resulting in an autism diagnosis in their offspring, has been observed clinically. Multiple patterns of MARA autoantibodies have been identified clinically, and differences in the severity of the autism phenotype based on the autoantibody pattern have been described. In this study we utilized our preclinical rat model to further elucidate the differential effects of MARA autoantibody exposure based on the known clinical patterns, including the originally identified pattern of lactate dehydrogenase A and B (LDHA/B) + collapsin response mediator protein 1 (CRMP1) + stress-induced phosphoprotein 1 (STIP1) as well as the newly described patterns of CRMP1+CRMP2, CRMP1 + guanine deaminase (GDA), and STIP1+ neuron-specific enolase (NSE). We found that, at postnatal day 2, the levels of brain-specific and serum cytokines/chemokines were altered based on the pattern of MARA autoantibody exposure. Further, we observed changes in the brain transcriptomic profiles that suggest cellular proliferation and differentiation changes due to MARA exposure.

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