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A nonsynonymous polymorphism in the human fatty acid amide hydrolase gene did not associate with either methamphetamine dependence or schizophrenia
Authors:Morita Yukitaka  Ujike Hiroshi  Tanaka Yuji  Uchida Naohiko  Nomura Akira  Ohtani Kyohei  Kishimoto Makiko  Morio Akiko  Imamura Takaki  Sakai Ayumu  Inada Toshiya  Harano Mutsuo  Komiyama Tokutaro  Yamada Mitsuhiko  Sekine Yoshimoto  Iwata Nakao  Iyo Masaomi  Sora Ichiro  Ozaki Norio  Kuroda Shigetoshi
Affiliation:Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
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.
Keywords:
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