Editorial: Can dysregulated myelination be linked to ADHD pathogenesis and persistence?

Area of Science:

• Neuroscience
• Developmental Biology
• Psychiatry

Background:

• Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder with persistent cognitive and emotional impairments.
• The etiology of ADHD is multifactorial, involving genetic, environmental, and neurobiological factors.

Discussion:

• Converging evidence suggests dysregulated myelination and associated alterations in neuronal plasticity are central to ADHD pathophysiology.
• Disrupted brain maturation, linked to myelination deficits, may explain the persistence of ADHD symptoms across the lifespan.
• This neurobiological concept integrates findings from epidemiology, genetics, epigenetics, neuroimaging, and experimental models.

Key Insights:

• Myelination deficits and altered neuronal plasticity are proposed as core mechanisms underlying ADHD onset and persistence.
• These neurobiological alterations disrupt normal brain maturation, leading to enduring cognitive and emotional impairments.
• The findings refine the understanding of ADHD's neurobiology, implicating developmental processes.

Outlook:

• Further research is needed to validate the proposed pathophysiologic mechanism of dysregulated myelination in ADHD.
• This refined understanding opens avenues for novel therapeutic interventions targeting myelination and neuronal plasticity.
• Investigating these mechanisms could lead to more effective, targeted treatments for individuals with ADHD.