Altered functional connectivity of the amygdaloid input nuclei in adolescents and young adults with autism spectrum disorder: a resting state fMRI study

作者：Rausch Annika^*; Zhang Wei; Haak Koen V; Mennes Maarten; Hermans Erno J; van Oort Erik; van Wingen Guido; Beckmann Christian F; Buitelaar Jan K; Groen Wouter B

来源：Molecular Autism, 2016, 7(1): 13.

DOI：10.1186/s13229-015-0060-x

• Amygdala
• Autism spectrum disorder
• Centromedial
• Connectivity
• Input-output
• Laterobasal
• Nuclei
• Social perception
• Superficial

Background: Amygdala dysfunction is hypothesized to underlie the social deficits observed in autism spectrum disorders (ASD). However, the neurobiological basis of this hypothesis is underspecified because it is unknown whether ASD relates to abnormalities of the amygdaloid input or output nuclei. Here, we investigated the functional connectivity of the amygdaloid social-perceptual input nuclei and emotion-regulation output nuclei in ASD versus controls.
Methods: We collected resting state functional magnetic resonance imaging (fMRI) data, tailored to provide optimal sensitivity in the amygdala as well as the neocortex, in 20 adolescents and young adults with ASD and 25 matched controls. We performed a regular correlation analysis between the entire amygdala (EA) and the whole brain and used a partial correlation analysis to investigate whole-brain functional connectivity uniquely related to each of the amygdaloid subregions.
Results: Between-group comparison of regular EA correlations showed significantly reduced connectivity in visuospatial and superior parietal areas in ASD compared to controls. Partial correlation analysis revealed that this effect was driven by the left superficial and right laterobasal input subregions, but not the centromedial output nuclei.
Conclusions: These results indicate reduced connectivity of specifically the amygdaloid sensory input channels in ASD, suggesting that abnormal amygdalo-cortical connectivity can be traced down to the socio-perceptual pathways.

• 出版日期2016-1-28