Display Settings:


Send to:

Choose Destination
Prog Neuropsychopharmacol Biol Psychiatry. 2010 May 30;34(4):692-6. doi: 10.1016/j.pnpbp.2010.03.026. Epub 2010 Mar 25.

Association of the manganese superoxide dismutase gene Ala-9Val polymorphism with clinical phenotypes and tardive dyskinesia in schizophrenic patients.

Author information

  • 1Department of Neurology, Tianjin Medical University General Hospital, Tianjin 300052, China.



Several recent studies that have investigated the genetic association between the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) and tardive dyskinesia (TD) have produced conflicting results. This study was to investigate whether this SNP was associated with clinical phenotypes and antipsychotic-induced tardive dyskinesia (TD) in schizophrenia in a genetically homogeneous Han Chinese inpatient population.


Genotyping was performed for the MnSOD gene Ala-9Val SNP in Chinese schizophrenia patients with (n=176) and without TD (n=346). The severity of TD was assessed using the abnormal involuntary movement scale (AIMS), and psychopathology using the Positive and Negative Syndrome Scale (PANSS).


The frequencies of genotypes and alleles did not differ significantly between schizophrenic patients with and without TD (both p>0.05). Also, there was no significant difference in the AIMS total score between the Val/Val and Ala allele carrier groups (p>0.05). However, the PANSS negative symptom subscore was significantly higher in patients with Val/Val genotype (21.8+/-7.3) than those with Ala alleles (20.1+/-7.7) (t=2.32, p=0.03).


While the MnSOD gene Ala-9Val polymorphism did not play a major role in the susceptibility to TD in schizophrenic patients, it might be associated with negative symptoms of schizophrenia.

Copyright 2010 Elsevier Inc. All rights reserved.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk