Prodynorphin (PDYN) binds to k-opioid receptors (KOPr; encoded by OPRK1) and is known to regulate dopaminergic tone, making this system important for drugs addiction.
OPRM1 alleles, genotypes and haplotypes from three psychiatrically characterized population samples (US Caucasian [USC, n=100], Finnish Caucasian [FC, n=324] and Southwestern American Indian [SAI, n=367]), were used to perform association and sib-pair linkage analyses with alcohol and drug dependence diagnoses.
A common single nucleotide polymorphism (SNP), A118G, in the mu-opioid receptor gene can affect opioid function and, consequently, has been suggested to contribute to individual variability in pain management and drug addiction.
A large body of evidence in both animal and human studies suggests that CB1R antagonism is highly effective for the treatment of obesity, metabolic disorders and drug addiction.
A number of intriguing parallels in drug-addicted cancers became apparent in a comparison of the two models: (i) overexpression of driver oncogenes as causes of acquired resistance; (ii) overexpression of driver oncogenes causing MEK-ERK hyperactivation under drug-free conditions; (iii) hyperactivation of the MEK-ERK pathway as critical to this drug addiction phenomenon; (iv) ongoing dependence on the oncogenic driver; and (v) morphologic changes in resistant cells under drug-free conditions.
A number of intriguing parallels in drug-addicted cancers became apparent in a comparison of the two models: (i) overexpression of driver oncogenes as causes of acquired resistance; (ii) overexpression of driver oncogenes causing MEK-ERK hyperactivation under drug-free conditions; (iii) hyperactivation of the MEK-ERK pathway as critical to this drug addiction phenomenon; (iv) ongoing dependence on the oncogenic driver; and (v) morphologic changes in resistant cells under drug-free conditions.
A number of intriguing parallels in drug-addicted cancers became apparent in a comparison of the two models: (i) overexpression of driver oncogenes as causes of acquired resistance; (ii) overexpression of driver oncogenes causing MEK-ERK hyperactivation under drug-free conditions; (iii) hyperactivation of the MEK-ERK pathway as critical to this drug addiction phenomenon; (iv) ongoing dependence on the oncogenic driver; and (v) morphologic changes in resistant cells under drug-free conditions.
A retrospective study was conducted in 938 MA-dependent patients who were recruited between February 2, 2008 and March 11, 2013, with social characteristics and drug-dependence history (duration of MA use, routes of drug administration, and daily dose were collected).
A single nucleotide polymorphism (SNP) in the human mu-opioid receptor gene (OPRM1A118G) has been widely studied for its association in a variety of drug addiction and pain sensitivity phenotypes; however, the extent of these adaptations and the mechanisms underlying these associations remain elusive.
A single-nucleotide polymorphism (SNP) within the OPRM1 gene, A118G, leading to an amino acid change (Asn40Asp) in the extracellular portion of the receptor, has been implicated in alcoholism as well as in drug addiction, pain sensitivity and stress response, and in animal and human studies relates to the alcohol-dependent phenotype as well as to the treatment response to the µ-opioid antagonist naltrexone.
A variant of the ADH1B gene (rs1229984 or rs1229984;rs750891770;s750891770" genes_norm="125;64129">Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug dependence.
A variant of the ADH1B gene (rs1229984 or rs1229984;rs750891770;s750891770" genes_norm="125;64129">Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug dependence.
A variant of the ADH1B gene (rs1229984 or rs1229984;rs750891770;s750891770" genes_norm="125;64129">Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug dependence.
A variant of the ADH1B gene (rs1229984 or rs1229984;rs750891770;s750891770" genes_norm="125;64129">Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug dependence.
A variant of the ADH1B gene (rs1229984 or rs1229984;rs750891770;s750891770" genes_norm="125;64129">Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug dependence.
A variant of the ADH1B gene (rs1229984 or rs1229984;rs750891770;s750891770" genes_norm="125;64129">Arg48His; previously referred to as Arg [*1] and His [*1]) has been reported to be associated with reduced rates of alcohol and drug dependence.
Accordingly, available nonclinical data and some clinical observations targeting 5-HT(2C) receptors may offer innovative translational strategies for combating drug dependence.This article is part of a Special Issue entitled: Brain Integration.
Accumulating clinical and preclinical evidence suggests that HINT1 may play an important role as a neuroplastic mediator in neuropsychiatric diseases, such as schizophrenia, inherited peripheral neuropathies, mood disorders, and drug addiction.
Although none of the SNPs achieved genome-wide association significance levels (defined as p<.000001), two genes probed with multiple SNPs (OPRM1 and CHRNA2) emerged as plausible candidates for a role in antisocial drug dependence after gene-based permutation tests.