Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease with the hallmark characteristics of pruritus, psychological stress, and sleep disturbance, all possibly associated with an increased risk of attention-deficit/hyperactivity disorder (ADHD). However, the etiology of the possible association between AD and ADHD is still not well understood. 2,4-dinitrochlorobenzene or corticosterone was used to evaluate the atopic symptom and its psychologic stress in the atopic mice model. Melatonin, corticotropin-releasing hormone, corticotropin-releasing hormone receptor, urocortin, proopiomelanocortin, adrenocorticotropic hormone, corticosterone, cAMP, cAMP response element-binding protein, dopamine and noradrenaline were analyzed spectrophotometrically, and the expression of dopamine beta-hydroxylase and tyrosine hydroxylase were measured by Western blotting or immunohistochemistry. AD-related psychological stress caused an increase in the levels of dopamine beta-hydroxylase and tyrosine hydroxylase, degradation of melatonin, hyper-activity of the hypothalamic-pituitary-adrenal axis, and dysregulation of dopamine and noradrenaline levels (ADHD phenomena) in the locus coeruleus, prefrontal cortex, and striatum of the AD mouse brain. Notably, melatonin administration inhibited the development of ADHD phenomena and their-related response in the mouse model. This study demonstrated that AD-related psychological stress increased catecholamine dysfunction and accelerated the development of psychiatric comorbidities, such as ADHD.
Highlights
attention-deficit/hyperactivity disorder (ADHD) is a common childhood disorder affecting around 7% of all children, and often persists into adulthood[1,2]
adrenocorticotropic hormone (ACTH) and the sympathetic nervous system stimulate the synthesis of adrenaline precursors by enhancing the activity of tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DβH), two enzymes involved in catecholamine synthesis[36,37,38]
We observed significantly increased cyclic adenosine monophosphate (cAMP) and pCREB expression in the locus coeruleus (LC); subchronic melatonin reduced cAMP and pCREB expression in DNCB-treated mice
Summary
ADHD is a common childhood disorder affecting around 7% of all children, and often persists into adulthood[1,2]. Considering immune-regulatory roles of the HPA axis and the sympathetic-adrenal-medullary systems, especially under stress, an aberrant responsiveness of these systems may increase susceptibility to allergic inflammation and may be a psycho-biological mechanism of stress-related aggravation of AD24,25. These ideas are supported by a study showing raised glucocorticoid and adrenocorticotropic hormone (ACTH) levels under stress in adults with AD, which indicate a dysfunctional HPA axis. The inattentive ADHD subtype was characterized by a trend towards a higher cortisol response than that observed in the controls[3,30,31] These reports suggest the significance of distinguishing the inattentive and combined subtypes in the diagnosis of ADHD. Several clinical studies have found associations between AD, ADHD, and attention deficits
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