A nonsynonymous polymorphism in the human fatty acid amide hydrolase gene did not associate with either methamphetamine dependence or schizophrenia

Yukitaka Morita, Hiroshi Ujike, Yuji Tanaka, Naohiko Uchida, Akira Nomura, Kyohei Ohtani, Makiko Kishimoto, Akiko Morio, Takaki Imamura, Ayumu Sakai, Toshiya Inada, Mutsuo Harano, Tokutaro Komiyama, Mitsuhiko Yamada, Yoshimoto Sekine, Nakao Iwata, Masaomi Iyo, Ichiro Sora, Norio Ozaki, Shigetoshi Kuroda

Research output: Contribution to journalArticlepeer-review

58 Citations (Scopus)

Abstract

Genetic contributions to the etiology of substance abuse and dependence are topics of major interest. Acute and chronic cannabis use can produce drug-induced psychosis resembling schizophrenia and worsen positive symptoms of schizophrenia. The endocannabinoid system is one of the most important neural signaling pathways implicated in substance abuse and dependence. The fatty acid amide hydrolase (FAAH) is a primary catabolic enzyme of endocannabinoids. To clarify a possible involvement of FAAH in the etiology of methamphetamine dependence/psychosis or schizophrenia, we examined the genetic association of a nonsynonymous polymorphism of the FAAH gene (Pro129Thr) by a case-control study. We found no significant association in allele and genotype frequencies of the polymorphism with either disorder. Because the Pro129Thr polymorphism reduces enzyme instability, it is unlikely that dysfunction of FAAH and enhanced endocannabinoid system induce susceptibility to either methamphetamine dependence/psychosis or schizophrenia.

Original languageEnglish
Pages (from-to)182-187
Number of pages6
JournalNeuroscience Letters
Volume376
Issue number3
DOIs
Publication statusPublished - 16-03-2005

All Science Journal Classification (ASJC) codes

  • General Neuroscience

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