病证结合驱动儿童ADHD共患病中西医结合诊疗的分子机制与临床转化研究进展OA

Attention deficit hyperactivity disorder(ADHD)is a common neurodevelopmental disorder in childhood.It has a high incidence and is often accompanied by a variety of comorbidities,which increases the complexity of treatment.Traditional Chinese medicine theory and molecular mechanism can explain the pathogenesis of ADHD and its comorbidity from different theoretical systems,and the two are interrelated and affect each other.Traditional Chinese medicine believes that its core symptoms are closely related to the dysfunction of Zang Fu organs and the imbalance of Yin and Yang,and the comorbidity is often caused by the further dysfunction of Zang Fu organs or the aggravation of the imbalance of Yin and Yang.Modern medical molecular mechanism research has revealed the molecular genetic basis of ADHD.It has found that many genes related to neurodevelopment are related to the pathogenesis of ADHD,involving the abnormalities of neurotransmitter system,such as dopamine,norepinephrine and 5-hydroxytryptamine.From the perspective of disease syndrome combination,this paper comprehensively uses the holistic concept of traditional Chinese medicine and the principle of syndrome differentiation and treatment,combined with the results of modern molecular biology research,to explore the pathogenesis of ADHD comorbidity in children.Starting from the basis of molecular genetics,this paper analyzes the genetic susceptibility and the abnormalities of neurotransmitter systems such as dopamine system,and expounds the core pathogenesis of traditional Chinese medicine,such as the imbalance of Yin and Yang and the interaction of phlegm and blood stasis,and points out the key roles of kidney essence deficiency,liver Yang hyperactivity and phlegm turbid obstruction in ADHD and its comorbidity.The pathogenesis and molecular mechanism of learning disorder,anxiety and depression disorder,oppositional defiant disorder and tic disorder in children with ADHD were further analyzed in detail,emphasizing the extended role of visceral dysfunction in these comorbidities and the influence of molecular mechanisms such as neurotransmitter imbalance and neural plasticity changes.