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Association of DISC1, BDNF, and COMT polymorphisms with exploratory eye movement of schizophrenia in a Chinese Han population

期刊

PSYCHIATRIC GENETICS
卷 26, 期 6, 页码 258-265

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/YPG.0000000000000138

关键词

brain-derived neurotrophic factor; catechol-O-methyl transferase; disrupted-in-schizophrenia-1; exploratory eye movement; schizophrenia

资金

  1. National Natural Science Foundation of China [81222017, 91232305]

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Background Previous studies suggested that exploratory eye movement (EEM) dysfunction appears to be a biological marker specific to schizophrenia, with an unknown molecular mechanism. Genetic studies indicate that disrupted-in-schizophrenia-1 (DISC1), brain-derived neurotrophic factor (BDNF), and catechol-O-methyl transferase (COMT) genes might be implicated in the etiology of schizophrenia, but not in all populations. Objectives The present study aimed to explore associations between these candidate genes and EEM endophenotypes for schizophrenia in a Chinese Han population. Methods EEM recordings were examined in 139 patients with schizophrenia and 143 healthy control participants. Results All five EEM parameters, responsive search score, cognitive search score, number of eye fixations, total eye scanning length, and mean eye scanning length, of schizophrenic patients differed significantly from those of healthy controls (P<0.001). The DISC1 Ser(704)Cys, BDNF Val(66)Met, and COMT Val(108)(/158)Met were genotyped in a total sample of 818 schizophrenic patients and 827 healthy control participants, including the above EEM samples. We found that DISC1 Cys(704) and BDNF Met(66) were associated with an increased risk of developing schizophrenia (P<0.001). Furthermore, responsive search score scores of BDNF Met/Met carriers were significantly lower than those of Val allele carriers (P=0.022), which remained modest after Bonferroni correction. Conclusion The BDNF Met(66)Met polymorphism might be associated with the EEM dysfunction of schizophrenia. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.

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