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Associations between autistic-like traits and polymorphisms in NFKBIL1.
- Source :
- Acta Neuropsychiatrica; Aug2019, Vol. 31 Issue 4, p220-229, 10p
- Publication Year :
- 2019
-
Abstract
- Objective: The immune system has been suggested to be associated with neuropsychiatric disorders; for example, elevated levels of cytokines and the inflammation-related transcription factor nuclear factor kappa-B (NF-κB) have been reported in individuals with autism spectrum disorder (ASD). The aim of this study was to investigate possible associations between autistic-like traits (ALTs) and single nucleotide polymorphisms (SNPs) in NFKB1 (encoding a subunit of the NF-κB protein complex) and NF-κB inhibitor-like protein 1 (NFKBIL1). Methods: The study was conducted in a cohort from the general population: The Child and Adolescent Twin Study in Sweden (CATSS, n = 12 319, 9–12 years old). The subjects were assessed by the Autism-Tics, ADHD, and Other Comorbidities Inventory. Five SNPs within the two genes were genotyped (NFKBIL1 : rs2857605, rs2239707, rs2230365 and rs2071592; NFKB1 : rs4648022). Results: We found significant associations for two SNPs in NFKBIL1 : rs2239707 showed a significant distribution of genotype frequencies in the case-control analysis both for all individuals combined and in boys only, and rs2230365 was significantly associated with the ALTs-module language impairment in boys only. Furthermore, we found nominal association in the case-control study for rs2230365, replicating earlier association between this SNP and ASD in an independent genome-wide association study. Conclusion: The shown associations between polymorphisms in NFKBIL1 and ALTs are supporting an influence of the immune system on neuropsychiatric symptoms. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 09242708
- Volume :
- 31
- Issue :
- 4
- Database :
- Complementary Index
- Journal :
- Acta Neuropsychiatrica
- Publication Type :
- Academic Journal
- Accession number :
- 137477369
- Full Text :
- https://doi.org/10.1017/neu.2019.18