A Study of Nuclear Transcription Factor-Kappa B in Childhood Autism

Background: Several children with autism show regression in language and social development while maintaining normal motor milestones. A clear period of normal development followed by regression and subsequent improvement with treatment, suggests a multifactorial etiology. The role of inflammation in autism is now a major area of study. Viral and bacterial infections, hypoxia, or medication could affect both foetus and infant. These stressors could upregulate transcription factors like nuclear factor kappa B (NF-kappa B), a master switch for many genes including some implicated in autism like tumor necrosis factor (TNF). On this hypothesis, it was proposed to determine NF-kappa B in children with autism. Methods: Peripheral blood samples of 67 children with autism and 29 control children were evaluated for NF-kappa B using electrophoretic mobility shift assay (EMSA). A phosphor imaging technique was used to quantify values. The fold increase over the control sample was calculated and statistical analysis was carried out using SPSS 15. Results: We have noted significant increase in NF-kappa B DNA binding activity in peripheral blood samples of children with autism. When the fold increase of NF-kappa B in cases (n = 67) was compared with that of controls (n = 29), there was a significant difference (3.14 vs. 1.40, respectively; p < 0.02). Conclusion: This finding has immense value in understanding many of the known biochemical changes reported in autism. As NF-kappa B is a response to stressors of several kinds and a master switch for many genes, autism may then arise at least in part from an NF-kappa B pathway gone awry.