Abnormal functional responses and reductions in functional connectivity associated with functional abnormalities of the posterior cingulate cortex (PCC) is one of the most consistent findings in individuals with autism spectrum disorders (ASD). However, the significance of such findings for the pathophysiology of autism is unclear. In this study, we investigated cellular neurochemistry with proton magnetic resonance spectroscopy imaging (1H-MRS) in both, anterior (ACC) and posterior (PCC) cingulate cortices, brain regions associated, with networks sub serving alerting and executive control of attention in patients with ASD. Compared to typical development (TD) group, the ASD group showed significantly higher N-acetyl-aspartate/choline (NAA/Cho) ratio in PCC and demonstrated the metabolic differences between anterior and posterior cingulated cortices as a contribution to the pathogenesis of autism. Furthermore, provide the first direct evidence of the relationship between abnormal metabolic activity and posterior cingulate cortex dysfunction in ASD.

Campus Ciencias de La Salud University of La Laguna Tenerife Spain

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