APOE2 allele increased in tardive dyskinesia

Authors

  • Jonathan Halford MD,

    1. Department of Medicine (Neurology), Duke University Medical Center, Durham, North Carolina, USA
    Current affiliation:
    1. Department of Neurology, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309,Charleston, SC 29425
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  • Gandis Mazeika MD,

    1. Department of Medicine (Neurology), Duke University Medical Center, Durham, North Carolina, USA
    Current affiliation:
    1. Sleep Medicine Northwest, 10564 Fifth Avenue NE, Suite 205, Seattle, WA 98125
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  • Susan Slifer MS,

    1. Department of Medicine (Section of Medical Genetics), Duke University Medical Center, Durham, North Carolina, USA
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  • Marcy Speer PhD,

    1. Department of Medicine (Section of Medical Genetics), Duke University Medical Center, Durham, North Carolina, USA
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  • Ann M. Saunders MD,

    1. Department of Medicine (Neurology), Duke University Medical Center, Durham, North Carolina, USA
    Current affiliation:
    1. Genetics Research, GlaxoSmithKline, Inc., Research Triangle Park, NC 27709
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  • Warren J. Strittmatter MD,

    1. Department of Medicine (Neurology), Duke University Medical Center, Durham, North Carolina, USA
    2. Department of Neurobiology, Duke University Medical Center, Durham, North Carolina, USA
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  • Joel C. Morgenlander MD

    Corresponding author
    1. Department of Medicine (Neurology), Duke University Medical Center, Durham, North Carolina, USA
    • Department of Medicine (Neurology), Duke University Medical Center, Durham, NC 27710

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Abstract

Ninety-seven inpatients with tardive dyskinesia (average AIMS score = 13), the majority of whom were schizophrenic, were studied. Forty patients were Caucasian, and 57 were African–American. The APOE genotypes of these patients were compared to previously published genotypes of controls and with previously published studies of APOE genotypes in patients with schizophrenia. There were no significant differences in APOE allele frequencies comparing the African–American tardive dyskinesia population and the African–American control groups. In contrast, significant (< 0.05) P values were obtained comparing the Caucasian tardive dyskinesia population to the Caucasian controls, when comparing allele frequencies and genotypic frequencies. This study suggests that Caucasians bearing an APOE2 allele are at increased risk of developing tardive dyskinesia, whereas African–Americans are not. APOE genotype-specific risks of both tardive dyskinesia and Alzheimer's disease that vary across populations could be due to recruitment of patients or controls or could be due to modifying effects of differing genetic or environmental backgrounds. The mechanism by which the APOE2 allele increases risk of tardive dyskinesia is not known. Further information about the mechanisms of increased risk of tardive dyskinesia could result in stratification of prescribing practices weighing the costs of medications against the relative risk of side effects. © 2005 Movement Disorder Society

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