TY - GEN
T1 - Association study of the tumor necrosis factor-α gene and its 1A receptor gene with methamphetamine dependence
AU - Nomura, A.
AU - Ujike, Hiroshi
AU - Tanaka, Y.
AU - Kishimoto, M.
AU - Otani, K.
AU - Morita, Y.
AU - Morio, A.
AU - Harano, M.
AU - Inada, T.
AU - Yamada, M.
AU - Komiyama, T.
AU - Hori, T.
AU - Sekine, Y.
AU - Iwata, N.
AU - Sora, I.
AU - Iyo, M.
AU - Ozaki, N.
AU - Kuroda, S.
PY - 2006/8
Y1 - 2006/8
N2 - Recent preclinical findings that repeated treatment with methamphetamine (METH) induced an increase in tumor necrosis factor-α (TNF-α) mRNA in some brain regions and that TNF-α blocked METH neurotoxicity and rewarding effects suggest TNF-α, a multifunctional pro-inflammatory cytokine, may be involved in METH dependence. We hypothesized that genetic polymorphisms of the TNF-α gene and its receptor genes may be associated with vulnerability to METH dependence. Genetic association of -308G>A and -857C>T in the promotor region of the TNF-α gene, and 36A>G in exon 1 of the TNF receptor 1A gene (TNFR-SF1A), were analyzed in patients with METH dependence (n = 185) and healthy controls (n = 221) in a Japanese population. No significant association of alleles or haplotypes of the TNF-α or TNFR-SF1A genes with METH dependence was found. Neither was any significant association of clinical phenotype with METH dependence found. These results suggest that genetic variations in the TNF-α gene and its receptor genes may not be involved in individual vulnerability to METH dependence.
AB - Recent preclinical findings that repeated treatment with methamphetamine (METH) induced an increase in tumor necrosis factor-α (TNF-α) mRNA in some brain regions and that TNF-α blocked METH neurotoxicity and rewarding effects suggest TNF-α, a multifunctional pro-inflammatory cytokine, may be involved in METH dependence. We hypothesized that genetic polymorphisms of the TNF-α gene and its receptor genes may be associated with vulnerability to METH dependence. Genetic association of -308G>A and -857C>T in the promotor region of the TNF-α gene, and 36A>G in exon 1 of the TNF receptor 1A gene (TNFR-SF1A), were analyzed in patients with METH dependence (n = 185) and healthy controls (n = 221) in a Japanese population. No significant association of alleles or haplotypes of the TNF-α or TNFR-SF1A genes with METH dependence was found. Neither was any significant association of clinical phenotype with METH dependence found. These results suggest that genetic variations in the TNF-α gene and its receptor genes may not be involved in individual vulnerability to METH dependence.
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U2 - 10.1196/annals.1369.011
DO - 10.1196/annals.1369.011
M3 - Conference contribution
C2 - 17105909
AN - SCOPUS:33749573646
SN - 1573316296
SN - 9781573316293
T3 - Annals of the New York Academy of Sciences
SP - 116
EP - 124
BT - Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity
PB - Blackwell Publishing Inc.
ER -