AI Article Synopsis
- Autism spectrum disorder (ASD) is linked to various factors including genetics and immune dysfunction, although its exact causes remain unclear.
- Researchers examined the expression of the lncRNA IFNG-AS1 and the IFNG gene in 50 children with ASD compared to 50 healthy controls, discovering significant changes in their expression levels.
- The findings suggest a disruption in the regulation of IFNG and IFNG-AS1 in ASD children, especially among males, which may contribute to chronic inflammation associated with the disorder and could lead to new treatment insights.
Article Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with different epidemiological, genetic, epigenetic, and environmental factors. Although its etiology is not fully understood, immune dysfunction is implicated in this disease. Recently, a large number of genes encoding long noncoding RNAs (lncRNAs) were discovered which act as positive or negative regulators of neighboring target genes. The lncRNA, Interferon gamma-antisense RNA (IFNG-AS1), regulates expression levels of the Interferon gamma (IFNG) gene. In the present study, we investigated expression of IFNG and IFNG-AS1 in 50 children with ASD (15 females and 35 males, mean age: 6 ± 1.4 years) and 50 healthy controls (14 females and 36 males, mean age: 6 ± 1.74 years) by real time PCR technique. The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P < 0.0001; Fold change = -0.143, P = 0.013, respectively). The IFNG expression level increase was more pronounced in male ASD children (Fold change = 1.621; p < 0.0001). Our data reveal a functional disruption in the interactive network of IFNG/IFNG-AS1 regulation, which could be a contributing factor in the chronic inflammatory aspect of ASD. Our findings can help understanding the underlying contributors to ASD pathogenesis and find novel treatment options for children with ASD.
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| http://dx.doi.org/10.1007/s11011-019-00510-4 | DOI Listing |
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