Combined Influences of Genetic Factors and Attention Deficit Hyperactivity Disorder on the Development of Dependence on
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Combined Influences of Genetic Factors and Attention Deficit Hyperactivity Disorder on the Development of Dependence on Synthetic Cannabinoids A. E. Gareeva,1,2 R. R. Sharafiev,1 E. A. Akhmetova,1 T. R. Nasibullin,2 Z. R. Fakhurtdinova,3 V. L. Yuldashev,1 and A. R. Asadullin1
Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 120, No. 2, Iss. 1, pp. 15–21, February, 2020. Original article submitted April 24, 2019. Accepted April 24, 2019. Objectives. To create a complex model of the individual risk of developing dependence on synthetic cannabinoids taking account of the combined influences of genetic predisposition and attention deficit hyperactivity disorder (ADHD). Materials and methods. A total of 146 male adolescents consuming synthetic cannabinoids and 136 healthy subjects (controls) were observed. Genetic studies assessed cases with the combination of these dependencies with ADHD. DNA was collected and six polymorphic loci of genes of the dopaminergic and serotoninergic systems were determined; results were analyzed using a series of special statistical methods. Results and conclusions. These data demonstrate the important role of the dopaminergic and serotoninergic systems in the pathogenesis of dependence on psychoactive substances and the significance of changes in the nucleotide sequences of the DRD2, SLC6A3, and HTR2A genes in the development of dependence on synthetic cannabinoids in males with ADHD. Keywords: polymorphous gene loci, genes, psychoactive substance dependence, synthetic cannabinoids, attention deficit hyperactivity disorder.
Results from a number of studies have shown that attention deficit hyperactivity disorder (ADHD) is associated with an increased risk of developing dependence on psychoactive substances (PAS) and nicotine [1], and the prevalence of this syndrome is significantly greater among PAS addicts than in the general population [1]. A high level of heritability has been observed for ADHD (from 0.71 to 0.73), along with a concentration of cases of PAS dependence within families. Furthermore, the risk of developing PAS dependence is known to be greater among the relatives of probands with ADHD than among the relatives of healthy people [1]. Overlap between ADHD and PAS dependence may be mediated by a common genetic basis [2]. However, the na-
ture of the pathogenetic mechanism underlying this overlap currently remains unclear. A whole set of neurobiological pathogenetic pathways are involved in both the development of ADHD and the development of dependence on PAS, including the dopaminergic and serotoninergic systems. Changes in the functioning of the dopaminergic system of the brain play a significant role in in the development of PAS dependence. Use of these substances has been shown to lead to increases in extracellular dopamine, mainly in the ventral striatum [1]. Chronic PAS consumption leads to changes in neuroadaptation processes and a deficit in the dopaminergic reward system (for example, decreased accessibility of DRD2 receptors), which is r
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