1. Iidaka T, Miyakoshi M, Harada T, Nakai T. {{White matter connectivity between superior temporal sulcus and amygdala is associated with autistic trait in healthy humans}}. {Neurosci Lett};2012 (Feb 29);510(2):154-158.
Growing evidence suggests that autistic traits, such as reduced social and communication skills, exist along a continuum between healthy and pathological conditions. Thus, functional and structural investigations of neuroanatomical substrates that significantly correlate with autistic tendency in healthy human subjects are critical for understanding this disorder. To accomplish this goal, we performed functional magnetic resonance imaging (fMRI) in combination with diffusion tensor imaging (DTI) in 30 healthy young subjects. The subjects were evaluated using the Autistic-Spectrum Quotient (AQ), which was designed to measure autistic traits in healthy and autistic spectrum disorder (ASD) subjects. Face-specific brain activation in the superior temporal sulcus (STS) and amygdala (AMG) was identified using fMRI and passive viewing of faces. In addition, probabilistic tractography performed in each subject by using DTI showed a white matter pathway between the face-specific regions of interest in the STS and AMG. The volume of connectivity between the STS and AMG correlated positively with the total AQ score (Spearman’s rho=0.38, p<0.05); however, among the AQ subscales, only imagination was significantly associated with the connectivity volume. These results suggest that healthy subjects with high autistic traits may show an increase in the white matter pathway that connects key regions involved in face processing.
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2. Zhang Y, Sun Y, Wang F, Wang Z, Peng Y, Li R. {{Downregulating the Canonical Wnt/beta-catenin Signaling Pathway Attenuates the Susceptibility to Autism-like Phenotypes by Decreasing Oxidative Stress}}. {Neurochem Res};2012 (Feb 29)
Although a growing body of evidence supports the importance of the Wnt/beta-catenin signaling pathway and oxidative stress in the pathogenesis of autism, it is unclear whether a relationship exists between the Wnt/beta-catenin pathway and oxidative homeostasis. The present study examines the effects of sulindac, a small molecule inhibitor of the Wnt/beta-catenin signaling pathway, on the oxidative status of rats that are prenatally exposed to valproic acid (VPA), which is used in an animal model of autism. Our data show that sulindac treatment downregulated the canonical Wnt/beta-catenin signaling pathway by enhancing the expression of Glycogen Synthase Kinase 3beta and attenuating the expression of beta-catenin in comparison to levels in VPA-treated rats. Concomitantly, a marker of lipid peroxidation, 4-hydroxynonenal, was reduced as well. Sulindac treatment ameliorated the pain threshold, repetitive/stereotypic activity, learning and memory abilities and behavioral abnormalities of rats in our autism model. Our working model suggests that the upregulation of the Wnt/beta-catenin signaling pathway induced by VPA administration during early pregnancy produces an imbalance of oxidative homeostasis that facilitates susceptibility to autism. This information may be instrumental in designing appropriate therapeutic regimens with small molecule inhibitors of the Wnt/beta-catenin pathway for the treatment of autism-like behavioral phenotypes.
