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.

Cite this article as: Öğütlü H, Kaşak M, Tutku Tabur S. Mitochondrial dysfunction in attention deficit hyperactivity disorder. Eurasian J Med., 2022;54(Suppl. 1), S187-S195.