Investigation of foxp2 gene in patients wi̇th diagnosis specific learning disorder by using next generation sequencing method

Aim: Spesific Learning Disorder (SLD) is an important reason for the difficulties faced by school children in academic and social fields. The etiology of SLD is not yet known. However, genetic and environmental factors developing on a neurobiological basis, and their interaction with each other, are thought to be effective in etiology. In this study, it was aimed to investigate the role of FOXP2 gene in SLD etiology. Material and Method: Our study was carried out as a cross-sectional study. The patient group consisted of 52 children and control group included 46 children. In addition to the interviews conducted according to the DSM-5 criteria; Spesific Learning Disorder Test Battery and The Schedule for Affective Disorders and Schizophrenia (SADS) for School-Age Children – Present and Lifetime Version (SADS-PL) with semi-structured diagnostic interview schedule were applied to all study groups. In addition, Sociodemographic Information Form, Anxiety and Related Disorders Screening-For Children and "Child Depression Scale" were filled in for the whole group. The FOXP2 gene variation in the patient and control groups was investigated by the next generation sequence analysis method. Results: Seventeen (17) variations in the FOXP2 gene were detected in the patient and control groups. There were 13 different variations in 42 patients (80.8%) in the patient group, and 4 different variations were found in 27 children (52.17%) in the control group. The variations associated with the FOXP2 gene were found as significantly higher in the patient group. Conclusion: In our study, FOXP2 variation was more common in children with SLD. However, it is not possible to say with certainty what the role of variations detected in the patient group is in the etiopathogenesis, because there is not enough data in this context in patients with SLD. Further studies are needed to determine the role of FOXP2 gene-related variations and its relationship with clinical parameters in the etiology of SLD.