Clinical Psychopharmacology and Neuroscience Papers in Press available online.

Ebru Ulu1, Esra Demirci 1,*, Elif Funda Sener2, Sevgi Ozmen1, Melike Kevser Gul1, Reyhan Tahtasakal2, Fatma Dal2
Erciyes University School of Medicine, Department of Child and Adolescent Psychiatry, Kayseri, Turkey, Erciyes University Genome and Stem Cell Center (GENKOK) / Erciyes University Faculty of Medicine Department of Medical Biology, Kayseri, Turkey
Objective: Pathways associated with glutamate receptors are known to play a role in the pathophysiology of attention-deficit hyperactivity disorder (ADHD). However, Cyclin-Dependent Kinase 5 (CDK5), Microtubule-Associated Protein-2 (MAP2), Guanylate KinaseAssociated Protein (GKAP), and Postsynaptic Density 95 (PSD95), all of which are biomarkers involved in neurodevelopmental processes closely related to glutamatergic pathways, have not previously been studied in patients with ADHD. The main purpose of this study was to evaluate the plasma levels of CDK5, MAP2, GKAP, and PSD95 in children with ADHD and investigate whether these markers have a role in the etiology of ADHD.
Methods: Ninety-six children with ADHD between 6 and 15 years of age and 72 healthy controls were included in the study. Five milliliters of blood samples were taken from all participants. The samples were stored at –80°C until analyzed by the enzyme-linked immunosorbent assay method.
Results: Statistically significantly lower CDK5 levels were observed in children with ADHD than in healthy controls (p= 0.037). The MAP2, GKAP, and PSD95 levels were found to be statistically significantly higher in the ADHD group than in healthy controls (p=0.012, p=0.009, and p=0.024, respectively). According to binary regression analysis, CDK5 and MAP2 levels were found to be predictors of ADHD.
Conclusion: In conclusion, we found that a close relationship existed between ADHD and glutamatergic pathways, and low levels of CDK5 and high levels of MAP2 and GKAP played a role in the etiopathogenesis of ADHD.
Accepted Manuscript [Submitted on 2023-01-16, Accepted on 2023-05-02]