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Objective: Attention deficit hyperactivity disorder (ADHD) is one of the most prevalent childhood disorders. Although disorders etiology and pathogenesis have remained unknown, several theories about ADHD development have been proposed and many researchers believe that it might be caused by both genetic and environmental factors. In this study we evaluated miR18a-5p, miR22-3p, miR24-3p, miR106b-5p, miR107, miR125b-5p and miR155a-5p levels in child and adolescent ADHD patients.
Method: The research sample consisted of a group of 52 ADHD patients, and 52 healthy volunteer controls. Total RNA was extracted from Peripheral Whole Blood using Tri-Reagent. The hsa-miR-26b-5p was used as endogenous control microRNA. The mixed RNAs generated from the control group were used as a Reference RNA sample.
Results: There was no significant difference in age and sex between the two groups (p>0.05). Mirna 18a-5p, 22-3p, 24-3p, 106b-5p and 107 levels were statistically significantly decreased in ADHD patients (p<0.05). Mirna 155a-5p levels were increased in patients group (p<0.05). In the ROC curve Mir 107 levels under 0.4480 were highly predictive (PPV: 70.6) for the disease state and negative predictive value was 86,5%.
Conclusion: We found decreased mir 18a-5p,mir 22-3p, mir 24-3p, mir 106b-5p and mir 107 levels in patients. Previous studies examined relationship between miR-18a and reported this can be an important susceptibility mechanism for stress- related disorders. Dysregulation of mir22, mir 106b, mir107and mir24 in schizophrenia, bipolar disorders and autism has been reported. MiR-107 also has been studied in traumatic brain injury and neurodegenerative disease and fronto temporal dementia. We found increased mir 155a-5p in ADHD patients. mir155 dysregulation in depression patients and also Increased mir155 levels during lithium treatment has been reported. There could be a close relationship between levels of circulating miRNAs and ADHD. If we could understand how the signaling pathways were arranged by miRNAs, impact on CNS development, function and pathology, this could improve our knowledge about ADHD etiology and treatment.