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Role of NAD+ Oxidative Stress and Tryptophan Metabolism in Autism Spectrum Disorders

机译:NAD +氧化应激和色氨酸代谢在自闭症谱系障碍中的作用

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摘要

Autism spectrum disorder (ASD) is a pervasive neuro-developmental disorder characterized by impaired social interaction, reduced/absent verbal and non-verbal communication, and repetitive behavior during early childhood. The etiology of this developmental disorder is poorly understood, and no biomarkers have been identified. Identification of novel biochemical markers related to autism would be advantageous for earlier clinical diagnosis and intervention. Studies suggest that oxidative stress-induced mechanisms and reduced antioxidant defense, mitochondrial dysfunction, and impaired energy metabolism (NAD+, NADH, ATP, pyruvate, and lactate), are major causes of ASD. This review provides renewed insight regarding current autism research related to oxidative stress, mitochondrial dysfunction, and altered tryptophan metabolism in ASD.
机译:自闭症谱系障碍(ASD)是一种普遍存在的神经发育障碍,其特征是社交互动受损,言语和非言语交流减少/缺乏以及幼儿期的重复行为。对这种发育障碍的病因了解甚少,并且尚未鉴定出任何生物标志物。鉴定与自闭症有关的新型生化标志物将有助于早期临床诊断和干预。研究表明,氧化应激诱导的机制和减少的抗氧化剂防御,线粒体功能障碍以及能量代谢受损(NAD + ,NADH,ATP,丙酮酸和乳酸)是ASD的主要原因。这篇综述提供了有关当前自闭症研究中与氧化应激,线粒体功能障碍和ASD中色氨酸代谢改变有关的最新见解。

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