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PLoS One. 2011 May 9;6(5):e19488. doi: 10.1371/journal.pone.0019488.

A study of nuclear transcription factor-kappa B in childhood autism.

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1
Department of Psychiatry, Osmania Medical College, Hyderabad, India.

Abstract

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-κB), 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-κB in children with autism.

METHODS:

Peripheral blood samples of 67 children with autism and 29 control children were evaluated for NF-κB 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-κB DNA binding activity in peripheral blood samples of children with autism. When the fold increase of NF-κB 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-κB 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-κB pathway gone awry.

PMID:
21573053
PMCID:
PMC3090385
DOI:
10.1371/journal.pone.0019488
[Indexed for MEDLINE]
Free PMC Article
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