注意缺陷多动障碍中的线粒体功能障碍。

Pub Date : 2022-12-01 DOI:10.5152/eurasianjmed.2022.22187
Hakan Öğütlü, Meryem Kaşak, Selin Tutku Tabur
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摘要

注意缺陷多动障碍是一种神经发育障碍,主要症状是注意力不集中、多动和冲动,从幼儿期开始出现。注意缺陷多动障碍的病因复杂,以神经生物学为基础,涉及早期发育过程中的遗传、环境和生物因素。注意力缺陷多动障碍的病因尚未完全明确,但有研究认为,氧化应激增加是注意力缺陷多动障碍可能的常见病因之一。氧化应激可导致细胞损伤、DNA 修复系统失灵和线粒体功能障碍。线粒体功能障碍被认为是导致精神疾病的一个易感因素。本文旨在回顾为评估注意缺陷多动障碍与线粒体功能障碍之间可能存在的关系而开展的研究,并系统地分析这些研究获得的数据。尽管与自闭症谱系障碍、精神分裂症和情绪障碍相比,有关注意缺陷多动障碍与线粒体功能障碍之间关系的研究较少,但有关注意缺陷多动障碍的研究却在不断增加。线粒体 DNA 拷贝数的增加可能会对遗传和环境因素导致的线粒体功能障碍产生一个补偿系统。线粒体 DNA 拷贝数可能会随着接受治疗的患者注意力缺陷多动障碍严重程度和注意力缺陷的减轻而减少,并可能对线粒体功能产生积极影响。本综述的文献数据表明,线粒体功能障碍可能是注意力缺陷多动障碍病理生理学中的一个关键因素。了解线粒体在注意缺陷多动障碍发病机制中的作用,可能会开发出新的诊断工具,并为注意缺陷多动障碍的治疗制定新的治疗策略。
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Mitochondrial Dysfunction in Attention Deficit Hyperactivity Disorder.

Attention deficit hyperactivity disorder is a neurodevelopmental disorder with primary symptoms of inattention, hyperactivity, and impulsivity, beginning in early childhood. Attention deficit hyperactivity disorder has a complex etiology based on neurobiological foundations, involving genetic, environmental, and biological factors in the early development process. The etiology of attention deficit hyperactivity disorder has not been completely clarified yet, but it has been suggested that increased oxidative stress is one of the possible common etiologies in attention deficit hyperactivity disorder. Oxidative stress can cause cellular damage, DNA repair system malfunction, and mitochondrial dysfunction. Mitochondrial dysfunction is thought to be a susceptibility factor in the development of psychiatric diseases. This article aims to review the research conducted to evaluate the possible relationship between attention deficit hyperactivity disorder and mitochondrial dysfunction and systematically examine the data obtained from these studies. Although studies considering the relationship between attention deficit hyperactivity disorder and mitochondrial dysfunction are less than those of autism spectrum disorder, schizophrenia, and mood disorders, studies on attention deficit hyperactivity disorder are increasing. A compensating system against mitochondrial dysfunction caused by hereditary and environmental factors may be generated by an increase in mitochondrial DNA copy number. Mitochondrial DNA copies may decrease with the reduction of attention deficit hyperactivity disorder severity and attention deficit in patients receiving treatment and may positively affect mitochondrial functions. The literature data of this review show that mitochondrial dysfunction could be a crucial factor in the pathophysiology of attention deficit hyperactivity disorder. Understanding mitochondrial contributions in the pathogenesis of attention deficit hyperactivity disorder may result in new diagnostic tools and the development of new therapeutic strategies for attention deficit hyperactivity disorder treatment.

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