J Psychiatry Neurosci 2010; 34(3): 195-198
Shusuke Numata, MD, PhD; Jun-ichi Iga, MD, PhD; Masahito Nakataki, MD; Shin’Ya Tayoshi, MD, PhD; Toshihito Tanahashi, MD, PhD; Mitsuo Itakura, MD, PhD; Shu-ichi Ueno, MD, PhD; Tetsuro Ohmori, MD, PhD
Numata, Iga, Nakataki, Tayoshi, Ohmori — Department of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima; Tanahashi, Itakura — Division of Genetic Information, Institute for Genome Research, The University of Tokushima, Tokushima; Ueno — Department of Community and Psychiatric Nursing, School of Health Sciences, The University of Tokushima, and the Department of Neuropsychiatry, Neuroscience, Ehime University Graduate School of Medicine, Ehime, Japan
Background: Pericentrin (PCNT) interacts with disruption-in-schizophrenia 1 (DISC1), a known genetic risk factor for schizophrenia, bipolar disorder and major depressive disorder (MDD). We sought to determine whether the PCNT gene is implicated in MDD.
Methods: We performed case–control association analyses in the Japanese population. We analyzed 9 single nucleotide polymorphisms (SNPs) in 173 patients with MDD and 348 healthy controls.
Results: We found a significant allelic association between 3 SNPs (rs3788265, rs2073376 and rs2073380) of the PCNT gene and MDD (p = 0.006, 0.005 and 0.021, respectively). After correction for multiple testing, 2 SNPs (rs3788265 and rs2073376) retained significant allelic associations with MDD. In addition, we found a significant association between the 2 marker haplotypes (r3788265 and rs2073376) and MDD (permutation p = 0.011).
Limitations: Our sample was small and comprised only Japanese participants. In addition, owing to the late onset of MDD, it is possible that the disorder will develop in at least some participants in our control group. Finally, we did not show how SNPs of the PCNT gene alter its function.
Conclusions: Our results suggest that genetic variations in the PCNT gene may play a significant role in the etiology of MDD in the Japanese population.
Submitted Mar. 5, 2008; Revised Jun. 11, Oct. 5, 15, 2008; Accepted Oct. 16, 2008
Acknowledgements: We thank all the volunteers who participated in this study and the physicians who helped us to obtain clinical data and blood samples. We thank Mrs. Akemi Okada and Mrs. Kazue Tugawa for their technical assistance. This work was supported by a Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Culture, Sports, Science and Technology and a Grant-in-Aid for Scientific Research from the 21st Century COE program, Human Nutritional Science on Stress Control, Tokushima, Japan.
Competing interests: None declared.
Contributors: Drs. Numata and Iga designed the study and acquired the data. Drs. Nakataki, Itakura, Ueno and Ohmori also acquired the data, which Drs. Numata, Nakataki, Tayoshi, Tanahashi, Ueno and Ohmori analyzed. Dr. Numata wrote the article, which all authors reviewed and approved for publication.
Correspondence to: Dr. S. Numata, Department of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-8-15 Kuramoto-cho Tokushima 770-8503, Japan; fax 81-886-33-7131; firstname.lastname@example.org