2022年8月23日付で、「自閉症スペクトラム障害のシグナル伝達経路における脂質分子」とした総説論文が、International Journal of Molecular Sciences (Impact Factor 6.208) に掲載されました。

　現代医学では自閉症の原因は分かっていません。我々は自閉症児における脂質代謝系の異常に着目し、分子生物学的手法からその異常病態を解明してきました。本研究の知見をもとに、自閉症児の未来に向けた新薬の開発に結び付けたいと願っています。

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Abstract

The signaling pathways associated with lipid metabolism contribute to the pathophysiology of autism spectrum disorder (ASD) and provide insights for devising new therapeutic strategies. Prostaglandin E2 is a membrane-derived lipid molecule that contributes to the developing ASD associated with canonical signaling. Cyclooxygenases-2 plays a key role in neuroinflammation and is implicated in the pathogenesis of neurodevelopmental diseases such as ASD. The endocannabinoid system maintains a balance between the inflammatory and redox status, and synaptic plasticity, and is a potential target for ASD pathophysiology. Redox signaling refers to the specific and usually reversible oxidation–reduction reactions, some of which are also involved in pathways accounting for the abnormal behavior observed in ASD. Redox signaling and redox status-sensitive transcription factors contribute to the pathophysiology of ASD. Cannabinoids regulate the redox balance by altering the levels and activity of antioxidant molecules via ROS-producing NADPH oxidase (NOX) and ROS-scavenging superoxide dismutase enzymes. These signaling cascades integrate a broad range of neurodevelopmental processes that may be involved in the pathophysiology of ASD. Based on these pathways, we highlight putative targets that may be used for devising novel therapeutic interventions for ASD.