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Mitochondrial Dysfunction in Attention Deficit Hyperactivity Disorder
Hakan Öğütlü1, Meryem Kaşak2, Selin Tutku Tabur3
1Department of Child and Adolescent Psychiatry, Cognitive Behavioral Psychotherapies Association, Ankara, Turkey.
Insights
Mitochondrial dysfunction may play a key role in attention deficit hyperactivity disorder (ADHD) pathophysiology. Research suggests that addressing mitochondrial issues could lead to new ADHD diagnostic tools and treatments.
Area of Science:
- Neurobiology
- Developmental Disorders
- Cellular Biology
Background:
- Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder with complex origins.
- Oxidative stress and subsequent mitochondrial dysfunction are implicated in ADHD etiology.
- Mitochondrial dysfunction is a known susceptibility factor for psychiatric disorders.
Purpose of the Study:
- To review existing research on the relationship between ADHD and mitochondrial dysfunction.
- To systematically examine data from studies investigating this connection.
- To explore the potential of mitochondrial function as a therapeutic target for ADHD.
Main Methods:
- Systematic literature review of studies on ADHD and mitochondrial dysfunction.
- Analysis of data concerning mitochondrial DNA copy number and its relation to ADHD severity.
- Examination of research on the impact of ADHD treatment on mitochondrial function.
Main Results:
- Evidence suggests mitochondrial dysfunction is a significant factor in ADHD pathophysiology.
- Increased mitochondrial DNA copy number may act as a compensatory mechanism.
- Decreased mitochondrial DNA copies correlate with reduced ADHD severity and improved function with treatment.
Conclusions:
- Mitochondrial dysfunction is a crucial element in the development of ADHD.
- Further understanding of mitochondrial roles can inform novel diagnostic and therapeutic strategies for ADHD.
- Targeting mitochondrial pathways may offer new avenues for ADHD treatment.
Abstract:
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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