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Tryptophan hydroxylase gene polymorphisms are not associated with suicide
Author(s) -
Ono Hisae,
Shirakawa Osamu,
Nishiguchi Naoki,
Nishimura Akiyoshi,
Nushida Hideyuki,
Ueno Yasuhiro,
Maeda Kiyoshi
Publication year - 2000
Publication title -
american journal of medical genetics
Language(s) - English
Resource type - Journals
eISSN - 1096-8628
pISSN - 0148-7299
DOI - 10.1002/1096-8628(20001204)96:6<861::aid-ajmg34>3.0.co;2-p
Subject(s) - tryptophan hydroxylase , serotonergic , genetics , genotype , fenfluramine , allele , biology , polymorphism (computer science) , poison control , gene , endocrinology , serotonin , medicine , receptor , environmental health
Several lines of evidence suggest a serotonergic dysfunction involved in the biological susceptibility of suicide. Abnormalities of serotonergic markers such as 5‐hydroxyindoleacetic acid and prolactin response to fenfluramine have been demonstrated in suicide subjects. Tryptophan hydroxylase (TPH), the rate‐limiting enzyme in serotonin biosynthesis, is one of the most important regulating factors in the serotonergic system. Recently, polymorphisms of the TPH gene have been identified and some of these polymorphisms have been suggested to be associated with suicide, but the results are still inconsistent. We examined whether the −6526A/G polymorphism in the promoter region and the 218A/C polymorphism in intron 7 of the TPH gene were associated with suicide using 132 Japanese suicide victims. No significant difference in genotype distribution and allele frequencies of these polymorphisms was found between the suicide victims and the controls. We concluded neither the −6526A/G polymorphism nor the 218A/C polymorphism of the TPH gene is likely to have a major effect on the susceptibility of suicide. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:861–863, 2000. © 2000 Wiley‐Liss, Inc.

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