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Variants in PDE11A and PDE1A are not associated with citalopram response

Molecular Psychiatry volume 12, pages 1061–1063 (2007)Cite this article

Recently, Wong et al.1 investigated an association between polymorphisms in phosphodiesterase (PDE) genes and antidepressant response in a Mexican-American population. Two single nucleotide polymorphisms (SNPs) were associated with remission in response to either fluoxetine or desipramine although sample sizes for remitter and nonremitter groups were of limited size. Association between the reported PDE gene SNPs and remission in response to antidepressants requires further investigation using larger sample sizes. We sought to replicate the response phenotype data for two SNPs, rs1549870 (PDE1A) and rs1880916 (PDE11A) in a similar ethnic group for the nonremitter vs remitter analysis in the Wong et al. study. Additionally, we examined this potential association in Non-Hispanic Caucasians and African-American samples.

Our sample was derived from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study, a large-scale prospective clinical trial involving 4041 adults with nonpsychotic major depressive disorder (MDD). Details regarding the STAR*D study have been extensively described elsewhere.2, 3 Briefly, severity of depression was assessed with the 16-item Quick Inventory of Depressive Symptomatology Self Report before and during up to 12 weeks of treatment with the selective serotonin reuptake inhibitor, citalopram. DNA from 1953 subjects were obtained from the STAR*D study. We used 1804 subjects undergoing ⩾42 days of citalopram treatment, and classified individuals as responders if they had a final Quick Inventory of Depressive Symptomatology Self Report score 50% reduced from baseline score. Remitters were defined as those with a final Quick Inventory of Depressive Symptomatology Self Report score ⩽5.4 We had 110 responders (87 remitters and 23 nonremitting responders) and 94 nonresponders among our 204 Hispanic Caucasians. We extended the Wong et al. findings to Non-Hispanic Caucasians, for which we had 689 responders (592 remitters and 97 nonremitting responders) and 417 nonresponders; and African Americans, for which we had 130 responders (100 remitters and 30 nonremitting responders) and 121 nonresponders. Genotypes of subjects were determined using 5′ nuclease (TaqMan) assays and an ABI PRISM 7900HT Sequence Detection System (Applied Biosystems, Foster City, CA, USA) using the manufacturer's recommended protocol. An unconditional logistic regression was used to examine associations between the two selected SNPs and (1) nonremitters vs remitters and (2) nonresponders vs responders in Hispanic-Caucasian, Non-Hispanic-Caucasian and African-American groups. Because we were attempting to replicate the Wong et al. findings, we used a significance threshold of 0.05.

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References

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Acknowledgements

This work was supported by the National Institute of Mental Health to SPH (MH072802), the State of New York (PJM) and Grant CA 94919 (SLS) from the National Cancer Institute. STAR*D was funded by NIMH via contract (N01MH90003) to the University of Texas Southwestern Medical Center at Dallas (A John Rush, PI).

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Authors and Affiliations

  1. Department of Psychiatry and Institute for Human Genetics, University of California, San Francisco, CA, USA

    K S Teranishi, H Garriock, J B Kraft, E J Peters & S P Hamilton

  2. Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA

    S L Slager, M S Reinalda & G D Jenkins

  3. Department of Psychiatry, New York State Psychiatric Institute, Columbia University College of Physicians and Surgeons, New York, NY, USA. E-mail: SteveH@lppi.ucsf.edu,

    P J McGrath

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  1. K S Teranishi
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  2. S L Slager
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  8. P J McGrath
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  9. S P Hamilton
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Teranishi, K., Slager, S., Garriock, H. et al. Variants in PDE11A and PDE1A are not associated with citalopram response. Mol Psychiatry 12, 1061–1063 (2007). https://doi.org/10.1038/sj.mp.4002074

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