Mitochondrial dysfunction and mitophagy in ADHD: Cellular and molecular mechanisms

Abstract

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by persistent, age-inappropriate levels of inattention and/or hyperactive-impulsive behaviors. Previous investigations reveal that disrupted mitochondrial physiological homeostasis may contribute to ADHD. Several factors, including environmental factors, metabolic dysregulation, oxidative stress, neuroinflammation, and genetic abnormalities, can lead to mitochondrial dysfunction and impaired mitophagic pathways. Several investigations have been established a connection between mitochondrial dysfunction in ADHD and variations in monoaminergic genes, including dopamine receptors, dopamine transporters, norepinephrine transporters, serotonin transporters, and synaptic genes. The interplay between mitochondrial homeostasis and mitophagy in ADHD provides a promising research area and understating this interaction may help in the investigation of pathophysiological mechanisms and the innovation of novel therapeutic approaches to ADHD. Accordingly, this review explores previous studies that have investigated the mitochondrial abnormalities and dysfunctions in mitophagy at the cellular and molecular level in the development of ADHD.

Keywords

• Mitophagy
• ADHD
• Mitochondrial dysfunction
• Neuroinflammation
• Oxidative stress
• Neuronal death