Balkan Journal of Medical Genetics

ASSOCIATION BETWEEN OBSESSIVE COMPULSIVE DISORDER AND TUMOR NECROSIS FACTOR-α GENE –308 (G>A) AND –850 (C>T) POLYMORPHISMS IN TURKISH CHILDREN
Lüleyap HU1, Onatoğlu D1, Tahiroğlu AY2, Alptekin D1,*, Yılmaz MB1, Çetiner S3, Pazarbaşı A1, Ünal İ4, Avcı A2
*Corresponding Author: Professor Dr. Davut Alptekin, Department of Medical Biology and Genetics, Medical Faculty, Çukurova University, 01330 Adana, Turkey; Tel.: +90-322-3386060/3498; Fax: +90-322-3386572; E-mail: alptekin@cu.edu.tr
page: 61

INTRODUCTION

Obsessive compulsive disorder (OCD), attention- deficit hyperactivity disorder (ADHD) and tic disorders are prepubertal symptom onset autoimmune neuropsychiatric disorders associated with basal ganglia abnormalities in which antibodies produced against Group A β hemolytic streptococcus (GABHS) infections cross react against neuron epitopes. These disorders are referred to as post streptococcal movement disorders [1,2]. Obsessive compulsive disorder may be triggered by stress, anxiety and infections (for example; GABHS infections) [3]. Comor-bidities, GABHS infections, obsessions and compulsions are characteristic features in the etiology of OCD [4,5]. Due to the damage of basal ganglia after a period following a GABHS infection, tics and obsessive compulsive symptoms occur in patients. Exacerbations of OCD are accompanied by unstable emotions, motoric hyperactivity and symptoms of anxiety [4]. The association between Sydenham’s chorea and streptococcus infections was first mentioned by Taranta and Stollerman in 1956 [6] but association between OCD and Sydenham’s chorea was discovered by Snider and Swedo [4] and Swedo et al. [7]. In the late 1980s, the National Institute of Mental Health reported increased obsessive-compulsive symptoms in Sydenham’s chorea patients [8]. In the following decades, clinicians and researchers continued to make studies for neuropsychiatric disorders [9]. Recent studies suggest that 50.0-80.0% of OCD cases have a childhood onset [10]. Childhood onset OCD patients usually have a positive history of childhood tonsillitis, tic disorders and more antistrep-tolysin O (ASO) titers than adult onset OCD patients [11]. In addition, obsessions and compulsions are common symptoms for both of them [12,13]. According to Walitza et al. [14], 1.0-3.0% of the general population suffers from OCD. Prevalence of OCD in adolescents is 0.4% [7]. Clinical studies indicated that males frequently have earlier age onset of OCD than girls [15]. It was indicated that boys are much more affected than girls (3:2 ratio) [10]. However, epidemiological studies have shown that the incidence of many prepubertal boys diagnosed with OCD is three times that of girls. In addition, it was detected that incidence of OCD in females increases after puberty [15]. The immune system of patients is affected in OCD. In the patient’s immune system, the B lymphocyte susceptible to the M group of antigens, kills them. After B lymphocyte activation, some of the susceptible B lymphocytes pass through the blood-brain barrier and associates with the cell membrane of neuron cells because of epitope similarity [16-19]. Neurons are destroyed by the patient’s autoimmunity apoptosis mechanism. The loss of neurons, especially in basal ganglia, leads to neuropshychiatric signs such as obsessions, compulsions or tics because the basal ganglia is part of the brain which is responsible for cognition controlling, movement coordination and voluntary movements. Tumor necrosis factor (TNF) is an important cytokine and also has an important role in the apoptosis mechanism of autoimmune diseases. It is expressed by the TNF-α gene. The aim of our study was to identify the influence of the TNF-α gene –308 (G>A) and –850 (C>T) polymorphisms on OCD. Despite other research studies, the relationship between neuropsychiatric disorders and GABHS infections are not yet completely clear. One reason for this uncertainty is due to the triggering of other existing factors [20].

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