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

Morita, Yukitaka; Ujike, Hiroshi; Tanaka, Yuji; Uchida, Naohiko; Nomura, Akihiro; 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

doi:10.1016/j.neulet.2004.11.050

Cited by 55 publications

(46 citation statements)

References 37 publications

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“…FAAH is one of the enzymes involved in the regulation of the endocannabinoid system and genetic variants affecting enzyme activity are therefore clear candidates for genetic susceptibility to MI in patients with heart failure. FAAH is a primary catabolizer of ECS and serves as a regulator of endogenous cannabinoid signalling in the brain 16,17 . SNP 385C/A in the FAAH causes amino acid exchange in the position 129 (proline to threonine) with established functional effect.…”

Section: Discussionmentioning

confidence: 99%

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Association of polymorphisms in the endocannabinoid system genes with myocardial infarction and plasma cholesterol levels

Chmelíková¹,

Pácal²,

Špinarová³

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aims. The aim of this study was to investigate the relationship between selected symptoms of chronic heart failure (myocardial infarction, plasma cholesterol level) and single nucleotide polymorphisms (SNPs) in the FAAH and CNR1 genes. Methods. A case -control study involving 155 patients with chronic heart failure and 169 age-and sex-matched healthy subjects. We detected SNPs 385 C/A (rs324420) in the FAAH and 1359 G/A (rs1049353) in the CNR1 genes using the polymerase chain reaction and restriction analysis. Genotype and allele frequencies were compared between patients and controls as well as between patients with and without myocardial infarction. Results. No significant differences in genotype or allelic frequencies between patients and controls were found (P > 0.05). Carriers of the FAAH A allele had a 2.37-fold increase in the risk of myocardial infarction (odds ratio 2.37, 95% confidence interval 1.36-6.93, P = 0.01). Homozygous carriers of genotype AA of CNR1 SNP 1359 had significantly higher plasma cholesterol levels than carriers of GG and GA genotypes in patients (P = 0.04). Conclusions.The study results suggest a role for allele A of the FAAH 385 variant as a risk factor for myocardial infarction. Genotype AA of CNR1 1359 variant probably affects plasma cholesterol levels. Pharmacological intervention in this system could modify the therapeutic approach to certain cardiovascular disorders.

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Section: Discussionmentioning

confidence: 99%

“…Chronic blockade of CB1 receptors in obese animal and humans reduces the symptoms of the metabolic syndrome (accumulation of fat, especially intra-abdominal fat, hypertriglyceridemia, low high density lipoprotein cholesterol, high arterial pressure, and high fasting glycaemia) (ref. 16 ). …”

Section: Discussionmentioning

confidence: 99%

Association of polymorphisms in the endocannabinoid system genes with myocardial infarction and plasma cholesterol levels

Chmelíková¹,

Pácal²,

Špinarová³

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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“…Sample 2: Unrelated subjects were recruited in Taipei included 140 methamphetaminedependent individuals diagnosed using DSM IV criteria [81] [82][83][84][85][86]. 240 matching Han Chinese normal controls denied any history of use of illegal drugs and denied any histories of psychotic symptoms.…”

Section: B) Asian Methamphetamine-dependencementioning

confidence: 99%

“Higher order” addiction molecular genetics: Convergent data from genome-wide association in humans and mice

Uhl

Drgon

Johnson

et al. 2008

Biochemical Pharmacology

127

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Family, adoption and twin data each support substantial heritability for addictions. Most of this heritable influence is not substance-specific. The overlapping genetic vulnerability for developing dependence on a variety of addictive substances suggests large roles for "higher order" pharamacogenomics in addiction molecular genetics. We and others have now completed genomewide association (GWA) studies of DNAs from individuals with dependence on a variety of addictive substances vs appropriate controls. Recently reported replicated GWA observations identify a number of genes based on comparisons between controls and European-American and African-American polysubstance abusers. Here we review the convergence between these results and data that compares control samples and a) alcohol dependent European Americans, b) methamphetamine dependent Asians and c) nicotine dependent samples from European backgrounds. We also compare these human data to quantitative trait locus (QTL) results from studies of addiction-related phenotypes in mice that focus on alcohol, methamphetamine and barbiturates. These comparisons support a genetic architecture built from largely-polygenic contributions of common allelic variants to dependence on a variety of legal and illegal substances. Many of the gene variants identified in this way are likely to alter specification and maintenance of neuronal connections. KeywordsAssociation genome scanning; substance dependence; microarray; pooled; neuronal connections * To whom correspondence should be addressed at: Molecular Neurobiology, Box 5180, Baltimore, MD 21224 phone: (410) 550-2843 x 146, fax: (410) 550-1535, guhl@intra.nida.nih.gov. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access A. Studies of human addiction vulnerabilitiesVulnerability to addictions is a complex trait with strong genetic influences that are largely shared by abusers of different legal and illegal addictive substances [1][2][3][4]. This conclusion comes from family, adoption and twin studies. Family studies clearly document that first degree relative (eg sibs) of addicts display greater risk for developing substance dependence than more distant relatives [1,5]. Adoption studies consistently find greater similarities between substance abuse phenotypes with biological relatives than with adoptive family members [1]. In twin studies, differences in concordance between genetically identical and fraternal twins also support heritability for vulnerability to addictions [3,[6][7][8][9][10][11][12]. Twin data allows quantitation of the amount, about 50%, of ad...

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“…Sipe et al (33) found that its homozygous form is strongly associated with both street-drug use and problem drug / alcohol use. However, we have found that there is no association between the Pro129Thr mutation of the FAAH gene and susceptibility to schizophrenia in a Japanese population (34). Possible involvement of the gene in negative symptoms of schizophrenia including cognitive function should be elucidated.…”

Section: Endocannabinoids In Cerebrospinal Fluid (Csf)mentioning

confidence: 75%

New Perspectives in the Studies on Endocannabinoid and Cannabis: Cannabinoid Receptors and Schizophrenia

Ujike

Morita

2004

J Pharmacol Sci

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Abstract. Cannabis consumption may induce psychotic states in normal individuals, worsen psychotic symptoms of schizophrenic patients, and may facilitate precipitation of schizophrenia in vulnerable individuals. Recent studies provide additional biological and genetic evidence for the cannabinoid hypothesis of schizophrenia. Examinations using [3 H]CP-55940 or [3 H]SR141716A revealed that the density of CB 1 receptors, a central type of cannabinoid receptor, is increased in subregions of the prefrontal cortex in schizophrenia. Anandamide, an endogenous cannabinoid, is also increased in the CSF in schizophrenia. A genetic study revealed that the CNR1 gene, which encodes CB 1 receptors, is associated with schizophrenia, especially the hebephrenic type. Individuals with a 9-repeat allele of an AAT-repeat polymorphism of the gene may have a 2.3-fold higher susceptibility to schizophrenia. Recent findings consistently indicate that hyperactivity of the central cannabinoid system is involved in the pathogenesis of schizophrenia or the neural mechanisms of negative symptoms.

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

Cited by 55 publications

References 37 publications

Association of polymorphisms in the endocannabinoid system genes with myocardial infarction and plasma cholesterol levels

Association of polymorphisms in the endocannabinoid system genes with myocardial infarction and plasma cholesterol levels

“Higher order” addiction molecular genetics: Convergent data from genome-wide association in humans and mice

New Perspectives in the Studies on Endocannabinoid and Cannabis: Cannabinoid Receptors and Schizophrenia

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