4.7 Article

Association of Transferrin Gene Polymorphism with Cognitive Deficits and Psychiatric Symptoms in Patients with Chronic Schizophrenia

期刊

JOURNAL OF CLINICAL MEDICINE
卷 11, 期 21, 页码 -

出版社

MDPI
DOI: 10.3390/jcm11216414

关键词

transferrin; genetic polymorphism; psychiatric symptoms; cognitive deficits; schizophrenia

资金

  1. National Natural Science Foundation of China [61673391]
  2. Psychosis project of the Beijing Key Laboratory [Z161100002616017]
  3. CAS International Cooperation Research Program [153111KYSB20190004]

向作者/读者索取更多资源

Recent literature has focused on impaired iron homeostasis in the pathophysiology of schizophrenia. This study investigated the correlation between transferrin gene polymorphism and cognitive deficits and clinical symptoms in schizophrenia. The results suggest that the rs3811655 polymorphism is related to cognitive performance, negative symptoms, and total psychiatric symptoms in patients with schizophrenia.
A large amount of recent literature has focused on impaired iron homeostasis in the pathophysiology of schizophrenia. Specifically, microarray analysis has illustrated associations between the transferrin locus and schizophrenia. To elaborate on the effects of transferrin on schizophrenia and its psychiatric phenotypes, our study aimed to investigate whether transferrin gene polymorphism was correlated with cognitive deficits and clinical symptoms in schizophrenia. We recruited 564 patients with chronic schizophrenia and 422 healthy controls (HCs) in a Han Chinese population, collected phenotypic data, and genotyped the rs3811655 polymorphism of the transferrin gene. Our results showed that the rs3811655 polymorphism was related to cognitive performance in both patients and HCs, as well as negative symptoms in patients (all p < 0.05), and patients carrying at least one G-allele showed worsened cognition/severe negative symptoms (all p < 0.05). Further analyses also found that the rs3811655 polymorphism in combination with cognition may exert small but significant contributions to the negative (beta = -0.10, t = -2.48, p < 0.05) or total psychiatric symptoms (beta = -0.08, t = -1.92, p < 0.05) in patients. Our findings indicated that the rs3811655 polymorphism may be implicated in the cognitive deficits of schizophrenia and HCs as well as psychiatric symptoms in patients, which suggested the possible iron regulatory mechanism in the pathology of schizophrenia.

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