Lower Availability of Mitochondrial Complex I in Anterior Cingulate Cortex in Autism: A Positron Emission Tomography Study
Yasuhiko Kato, Masamichi Yokokura, Toshiki Iwabuchi, Chihiro Murayama, Taeko Harada, Takafumi Goto, Taishi Tamayama, Yosuke Kameno, Tomoyasu Wakuda, Hitoshi Kuwabara, Seico Benner, Atsushi Senju, Hideo Tsukada, Sadahiko Nishizawa, Yasuomi Ouchi, Hidenori Yamasue
Abstract
OBJECTIVE: Mitochondrial dysfunction has been implicated in the pathophysiology of autism spectrum disorder (ASD) in previous studies of postmortem brain or peripheral samples. The authors investigated whether and where mitochondrial dysfunction occurs in the living brains of individuals with ASD and to identify the clinical correlates of detected mitochondrial dysfunction. METHODS: F]BCPP-EF PET measurements. Individuals with mitochondrial disease were excluded by clinical evaluation and blood tests for abnormalities in lactate and pyruvate levels. RESULTS: F]BCPP-EF availability in the anterior cingulate cortex was significantly correlated with the more severe ASD core symptom of social communication deficits. CONCLUSIONS: This study provides direct evidence to link in vivo brain mitochondrial dysfunction with ASD pathophysiology and its communicational deficits. The findings support the possibility that mitochondrial electron transport chain complex I is a novel therapeutic target for ASD core symptoms.