ADHD from a Psychoneuroimmunology Perspective: The Role of Chronic Stress and Neuroinflammation

Attention-Deficit/Hyperactivity Disorder (ADHD) is typically conceptualized as a neurodevelopmental condition marked by persistent inattention, hyperactivity, and impulsivity. While cognitive and neurochemical models have advanced understanding and treatment, they do not fully explain the marked variability in symptom expression, emotional dysregulation, or inconsistent treatment outcomes. Emerging evidence suggests that biological responses to chronic stress may play a meaningful role in these patterns. Drawing on psychoneuroimmunology (PNI), this thesis examines how chronic stress–related immune activation interacts with dopaminergic systems implicated in ADHD. Particular focus is placed on hypothalamic–pituitary–adrenal (HPA) axis dysregulation, altered diurnal cortisol secretion, and elevations in pro-inflammatory cytokines such as IL-6, TNF-α, and CRP. These pathways may disrupt prefrontal and striatal dopamine signaling, contributing to attentional difficulties and emotional dysregulation. Integrating current evidence from stress physiology, neuroimmunology, and dopamine research, this work proposes that ADHD can be understood, in part, as a pattern of allostatic dysregulation, in which chronic stress and low-grade inflammation reinforce neural vulnerability. This perspective highlights the relevance of neuroimmune markers for explaining symptom heterogeneity and suggests potential benefit in extending ADHD management to include approaches that target stress regulation and inflammatory processes.