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Mediators of Inflammation
Volume 2011 (2011), Article ID 785265, 10 pages
Research Article

NF- B Signaling in the Brain of Autistic Subjects

Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA

Received 23 June 2011; Accepted 18 August 2011

Academic Editor: Giuseppe Valacchi

Copyright © 2011 Mazhar Malik et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Autism is a neurodevelopmental disorder characterized by problems in communication, social skills, and repetitive behavior. Recent studies suggest that apoptotic and inflammatory mechanisms may contribute to the pathogenesis of this disorder. Nuclear factor- B (NF- B) is an important gene transcriptional factor involved in the mediation of inflammation and apoptosis. This study examined the activities of the NF- B signaling pathway in the brain of autistic subjects and their age-matched controls. The NF- B activation is also determined in the brain of BTBR mice, which is a promising animal model for study of pathogenic mechanisms responsible for autism. Our results showed that the level of IKK kinase, which phosphorylates the inhibitory subunit I B , is significantly increased in the cerebellum of autistic subjects. However, the expression and phosphorylation of I B are not altered. In addition, our results demonstrated that the expression of NF- B (p65), and the phosphorylation/activation of NF- B (p65) at Ser536 are not significantly changed in the cerebellum and cortex of both autistic subjects and BTBR mice. Our findings suggest that the NF- B signaling pathway is not disregulated in the brain of autistic subjects and thus may not be significantly involved in the processes of abnormal inflammatory responses suggested in autistic brain.