title: A nonsynonymous polymorphism in the human fatty acid amide hydrolase gene did not associate with either methamphetamine dependence or schizophrenia.
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.
authors.affiliation: Department of Neuropsychiatry, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
authors.forename: Yukitaka
authors.initials: Y
authors.lastname: Morita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ujike
authors.forename: Yuji
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Naohiko
authors.initials: N
authors.lastname: Uchida
authors.forename: Akira
authors.initials: A
authors.lastname: Nomura
authors.forename: Kyohei
authors.initials: K
authors.lastname: Ohtani
authors.forename: Makiko
authors.initials: M
authors.lastname: Kishimoto
authors.forename: Akiko
authors.initials: A
authors.lastname: Morio
authors.forename: Takaki
authors.initials: T
authors.lastname: Imamura
authors.forename: Ayumu
authors.initials: A
authors.lastname: Sakai
authors.forename: Toshiya
authors.initials: T
authors.lastname: Inada
authors.forename: Mutsuo
authors.initials: M
authors.lastname: Harano
authors.forename: Tokutaro
authors.initials: T
authors.lastname: Komiyama
authors.forename: Mitsuhiko
authors.initials: M
authors.lastname: Yamada
authors.forename: Yoshimoto
authors.initials: Y
authors.lastname: Sekine
authors.forename: Nakao
authors.initials: N
authors.lastname: Iwata
authors.forename: Masaomi
authors.initials: M
authors.lastname: Iyo
authors.forename: Ichiro
authors.initials: I
authors.lastname: Sora
authors.forename: Norio
authors.initials: N
authors.lastname: Ozaki
authors.forename: Shigetoshi
authors.initials: S
authors.lastname: Kuroda
mesh_terms: D000328:Adult; D017668:Age of Onset; D000581:Amidohydrolases / Q000235:genetics*; D000595:Amino Acid Sequence / Q000235:genetics; D019943:Amino Acid Substitution / Q000235:genetics; D019969:Amphetamine-Related Disorders / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics*; D063385:Cannabinoid Receptor Modulators / Q000378:metabolism*; D016022:Case-Control Studies; D004252:DNA Mutational Analysis; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005820:Genetic Testing; D005838:Genotype; D006801:Humans; D007564:Japan / Q000453:epidemiology; D008297:Male; D008694:Methamphetamine / Q000009:adverse effects; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D011110:Polymorphism, Genetic / Q000235:genetics*; D012559:Schizophrenia / Q000201:enzymology / Q000453:epidemiology / Q000235:genetics*; D000099252:Fatty Acid Amide Hydrolases
chemical_list: D000581:Amidohydrolases; D063385:Cannabinoid Receptor Modulators; D008694:Methamphetamine; D000099252:Fatty Acid Amide Hydrolases