Abstract
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.
| Original language | English |
|---|---|
| Title of host publication | Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity |
| Subtitle of host publication | Cocaine, GHB, and Substituted Amphetamines |
| Publisher | Blackwell Publishing Inc. |
| Pages | 116-124 |
| Number of pages | 9 |
| ISBN (Print) | 1573316296, 9781573316293 |
| DOIs | |
| Publication status | Published - 01-01-2006 |
Publication series
| Name | Annals of the New York Academy of Sciences |
|---|---|
| Volume | 1074 |
| ISSN (Print) | 0077-8923 |
| ISSN (Electronic) | 1749-6632 |
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All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Biochemistry, Genetics and Molecular Biology(all)
- History and Philosophy of Science
Cite this
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Association study of the tumor necrosis factor-α gene and its 1A receptor gene with methamphetamine dependence. / Nomura, A.; Ujike, Hiroshi; Tanaka, Y.; Kishimoto, M.; Otani, K.; Morita, Y.; Morio, A.; Harano, M.; Inada, T.; Yamada, M.; Komiyama, T.; Hori, T.; Sekine, Y.; Iwata, N.; Sora, I.; Iyo, M.; Ozaki, N.; Kuroda, S.
Cellular and Molecular Mechanisms of Drugs of Abuse and Neurotoxicity: Cocaine, GHB, and Substituted Amphetamines. Blackwell Publishing Inc., 2006. p. 116-124 (Annals of the New York Academy of Sciences; Vol. 1074).Research output: Chapter in Book/Report/Conference proceeding › Conference contribution
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 - 2006/1/1
Y1 - 2006/1/1
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.
UR - http://www.scopus.com/inward/record.url?scp=33749573646&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33749573646&partnerID=8YFLogxK
U2 - 10.1196/annals.1369.011
DO - 10.1196/annals.1369.011
M3 - Conference contribution
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 -