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Genetic psychiatry No association between DNA methylation in BDNF gene and schizophrenia patients in Turkish population

derived neurotrophic factor (BDNF)—Epigenetic regulation in unipolar and bipolar affective disorder. OBJECTIVE: A number of studies on eye movement dysfunction in patients with psychiatric disease have been published. Glutamatergic neurotransmission mediated by the NMDA receptor is involved in the pathophysiology of schizophrenia and some neurological diseases 1. The frontal-thalamic-cerebellar circuit has been implicated in eye movements. The presence of eye-tracking abnormalities among schizophrenia patients and their biological correlates has been reported by numerous investigators examining smooth-pursuit and saccadic eye-movement measures, as well as measures of motion perception 2. An association between eye-tracking abnormalities and NMDA receptor antagonism is important because it indicates which neurophysiological mechanisms are related to eye-tracking abnormalities. There is strong evidence that eye-tracking abnormalities are related to genetic risk for schizophrenia 3 ; thus, a relationship between eye tracking and NMDA antagonism may also help us understand the biological underpinnings of disease vulnerability. On the other hand, the behavioral and pharmacological effects of the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist ketamine have been used to study important aspects of psychotomimetic action in humans. Several lines of evidence support the use of ketamine as a pharmacological model of schizophrenia. Schizophrenia patients administered subanesthetic doses of ketamine experience a brief exacerbation of positive, cognitive, and possibly negative symptoms. Ketamine also appears to provoke psychotic symptoms specific to a patient's disease history. Imaging studies have shown that ketamine changes the neuronal activity in areas thought to be involved in the pathophysiology of schizophrenia, including the medial frontal and anterior cingulate cortex, the hippocampus, and the cerebellum. Other studies have shown that ketamine causes schizophrenia-like positive, negative, and cognitive symptoms in normal healthy volunteers including deficits in sensory processing and eye-tracking performance. The non-competitive N-methyl-D-aspartate receptor antagonist ketamine leads to transient psychosis-like symptoms and impairments in oculomotor performance in healthy volunteers. In the literature, as far as we know, all studies have been conducted with specific tools (infrared oculography etc.) and special units for saccadic eye movements. In our study, we aimed to investigate the relationship between vertical eye position (VEP) and psychopathology via a scale designed by us. METHOD: Patients with the diagnosis of a psychiatric disorder (n=228) and control subjects (n=340) were included into the study. All subjects gave written informed consent in accordance with guidelines from the institutional review board of the GATA Haydarpasa Training Hospital. Subjects underwent a medical history, a physical examination, and laboratory tests, including a …