Examination of neuroplasticity and neuroprotection process in children with attention deficit hyperactivity disorder

Although the reason for attention deficit and hyperactivity disorder is not known exactly, with inhibitor effect of dopaminergic and noradrenergic activities, disorder in catecholamine metabolism in cerebral cortex is the most possible cause of ADHD. Neurobiological factors play an important role in the ethology of ADHD. However, the biological markers effecting the prognosis and treatment of ADHD are very limited. This study was planned to be conducted with the inclusion of 30 children who applied to Dicle University, Medicine Faculty, Psychiatry Polyclinic, and were diagnosed with ADHD yet without any systemic disease; and 30 healthy children. The serum levels of glial fibrillary acidic protein (GFAP), nogo-A, ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) and TAR DNA binding protein (TDP-43) were determined by Enzyme-linked immunosorbent assay (ELISA). In our study, it was found that serum levels of UCH-L1 and TDP-43 levels were statistically significantly higher in ADHD children than those of control group. Similarly, Nogo-A and GFAP levels were also found to be statistically significantly high in ADHD group. It can be suggested that neuroplasticity disorders are associated with ADHD and the levels of TDP-43 and UCH-L1 can ease the early diagnosis of ADHD to a great extent. Nevertheless, the cerebrospinal fluid levels of TDP-43 and UCH-L1 are yet unclear in children with ADHD; therefore, this issue deserves further investigation. In addition, GFAP and Nogo-A levels can be an evidence of neuroplasticity, microglial and astroglial changes in ADHD.