Addiction genetics最新文献

{"title":"Molecular Genetic Testing in Pain and Addiction: Facts, Fiction and Clinical Utility","authors":"K. Blum, M. Hauser, J. Fratantonio, R. Badgaiyan","doi":"10.1515/addge-2015-0001","DOIUrl":"https://doi.org/10.1515/addge-2015-0001","url":null,"abstract":"Abstract The Brain Reward Cascade (BRC) is an interaction of neurotransmitters and their respective genes to control the amount of dopamine released within the brain. Any variations within this pathway, whether genetic or environmental (epigenetic), may result in addictive behaviors as well as altered pain tolerance. While there are many studies claiming a genetic association with addiction and other behavioral infractions, defined as Reward Deficiency Syndrome (RDS), not all are scientifically accurate and in some case just wrong. Albeit our bias, we discuss herein the facts and fictions behind molecular genetic testing in RDS (including pain and addiction) and the significance behind the development of the Genetic Addiction Risk Score (GARSPREDX™), the first test to accurately predict one’s genetic risk for RDS.","PeriodicalId":90086,"journal":{"name":"Addiction genetics","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1515/addge-2015-0001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67109602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gender Differences in Alcohol Metabolizing Hepatic Enzyme Genotypes in Korean Patients with Alcohol Dependence","authors":"Jin-Seong Lee, Sung-Gon Kim, Sae-Heon Jang, W. Byun, I. Hwang, Chang-Soo Kim, Seong-Yeon Kim, Hyun-Sook Lee, Young-Hui Yang, D. Oslin","doi":"10.2478/addge-2013-0001","DOIUrl":"https://doi.org/10.2478/addge-2013-0001","url":null,"abstract":"Abstract There are a number of epidemiological studies concerning the gender differences in the genetic etiology of alcohol dependence (AD), with ADH2 and ALDH2 being strong candidates. The purpose of this study was to investigate gender differences in frequencies of ADH2 and ALDH2 genotypes in AD patients and in a normal control (NC) group of Koreans. Study subjects consisted of 228 AD patients (180 males, 48 females) and 138 NC (79 males, 59 females). For both male and female subjects, the frequency of the ADH2*1/1 genotype was significantly higher in AD patients compared to the NC group. However, the effect size of the ADH2*1/1 genotype on AD was much larger in females than in males. Furthermore, the ALDH2*1/1 genotype was positively associated with AD in male subjects but negatively associated with AD in female patients. Interestingly, AD in males was primarily determined by ALDH2 enzyme activity (92%), whereas female AD was primarily determined by ADH2 enzyme activity (60.4%). These results suggest that risk for the development of AD in males is mainly associated with the ALDH2*1/1 genotype, while in female patients, the ADH2*1/1 genotype was more highly associated with risk of AD. Overall, it is evident that gender differences associated with genetic risks for AD are present.","PeriodicalId":90086,"journal":{"name":"Addiction genetics","volume":"11 1","pages":"12 - 18"},"PeriodicalIF":0.0,"publicationDate":"2013-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2478/addge-2013-0001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69088755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethanol Withdrawal-Associated Drinking and Drinking in the Dark: Common and Discrete Genetic Contributions","authors":"J. Crabbe, P. Metten, Lawrence C. Huang, Jason P. Schlumbohm, Stephanie E. Spence, A. Barkley-Levenson, D. Finn, J. Rhodes, A. Cameron","doi":"10.2478/addge-2012-0002","DOIUrl":"https://doi.org/10.2478/addge-2012-0002","url":null,"abstract":"Ethanol Withdrawal-Associated Drinking and Drinking in the Dark: Common and Discrete Genetic Contributions Individual mice differ in the dose of ethanol they will ingest voluntarily when it is offered during limited access periods in the circadian dark, a phenotype called drinking in the dark (DID). Substantial genetic variation in DID has been reported across a few standard inbred mouse strains, and a line of High Drinking in the Dark (HDID) mice has been established through selective breeding on the blood ethanol concentration (BEC) they attain at the end of a drinking session. Here, we report ethanol DID data for 23 inbred mouse strains, including 11 not previously reported, corroborating the genetic contributions to this trait. We also report data on a different ethanol drinking trait, the increased intake seen after multiple cycles of chronic intermittent exposure to ethanol vapor (CIE). Drinking escalated significantly during ethanol withdrawal. However, HDID mice and their HS controls showed equivalent escalation during withdrawal, demonstrating that withdrawal-associated drinking escalation is not a clear genetic correlate of selection on DID. Across inbred strains, DID is substantially genetically correlated with previously-published twobottle ethanol preference drinking data assessed under conditions of continuous ethanol access. Although inbred strain data for withdrawalassociated drinking are not available, the current pattern of results suggests that withdrawal-associated drinking is genetically distinct from DID, while genetic contributions to DID and two-bottle preference drinking are substantially similar.","PeriodicalId":90086,"journal":{"name":"Addiction genetics","volume":"1 1","pages":"11 - 3"},"PeriodicalIF":0.0,"publicationDate":"2012-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2478/addge-2012-0002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69088711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethanol Withdrawal-Associated Drinking and Drinking in the Dark: Common and Discrete Genetic Contributions.","authors":"John C Crabbe,&nbsp;Pamela Metten,&nbsp;Lawrence C Huang,&nbsp;Jason P Schlumbohm,&nbsp;Stephanie E Spence,&nbsp;Amanda M Barkley-Levenson,&nbsp;Deborah A Finn,&nbsp;Justin S Rhodes,&nbsp;Andy J Cameron","doi":"10.2478/addge-2012-0002,","DOIUrl":"https://doi.org/10.2478/addge-2012-0002,","url":null,"abstract":"<p><p>Individual mice differ in the dose of ethanol they will ingest voluntarily when it is offered during limited access periods in the circadian dark, a phenotype called drinking in the dark (DID). Substantial genetic variation in DID has been reported across a few standard inbred mouse strains, and a line of High Drinking in the Dark (HDID) mice has been established through selective breeding on the blood ethanol concentration (BEC) they attain at the end of a drinking session. Here, we report ethanol DID data for 23 inbred mouse strains, including 11 not previously reported, corroborating the genetic contributions to this trait. We also report data on a different ethanol drinking trait, the increased intake seen after multiple cycles of chronic intermittent exposure to ethanol vapor (CIE). Drinking escalated significantly during ethanol withdrawal. However, HDID mice and their HS controls showed equivalent escalation during withdrawal, demonstrating that withdrawal-associated drinking escalation is not a clear genetic correlate of selection on DID. Across inbred strains, DID is substantially genetically correlated with previously-published two-bottle ethanol preference drinking data assessed under conditions of continuous ethanol access. Although inbred strain data for withdrawal-associated drinking are not available, the current pattern of results suggests that withdrawal-associated drinking is genetically distinct from DID, while genetic contributions to DID and two-bottle preference drinking are substantially similar.</p>","PeriodicalId":90086,"journal":{"name":"Addiction genetics","volume":"1 ","pages":"3-11"},"PeriodicalIF":0.0,"publicationDate":"2012-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3923583/pdf/nihms540931.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32123574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Addiction Genetics: A Harbinger of Advanced Research and New Treatment for Addiction","authors":"D. Choi","doi":"10.2478/addge-2012-0001","DOIUrl":"https://doi.org/10.2478/addge-2012-0001","url":null,"abstract":"Drug abuse and addiction cause immensely challenging problems in our society, affecting more than 5% of the worldwide population and costing approximately 3% of the world gross domestic product [3,10,11]. Legal, educational and social systems are limited in their capacity to reduce the socio-economical burdens of addiction. At the same time, currently available pharmaceutical medications are not sufficient to treat diverse types of addiction [2]. Contributing to this problem is our lack in understanding of this abnormal human behavior, so we oftenraise fundamental scientific questions. Why are some individuals more susceptible to abusing substances such as alcohol, nicotine, cocaine, methamphetamine, heroin, etc., while others are resilient? Are there common genetic or environmental factors that contribute to addiction? How do inherited components interact with environmental factors in the addiction process? Are there unique attributes to each form of addiction? Do non-substance addictions, including gambling or internet addiction, share common neurobiological or genetic features with other substance-addictions? Are there better ways to treat addiction? With the advent of new tools in genetics, genomics and epigenetics, we have renewed hope for answering the above questions. Genetic contributions to addiction have been a hallmark of addiction research in the last decade [4], yet pinpointing direct relationships between genes and addictive processes still remains elusive. Because of heterogeneity in the genetics of addictive behaviors, there is a constant need to develop more advanced and translatable addiction disease models using primates, rodents, zebrafish, Drosophila, and C. elegans. Genetic study does not simply refer to mutated DNA in genes, it also comprises drug-induced transcriptional changes through epigenetic mechanisms [12] altering neuroadaptation and behavior in a long-lasting manner. Very recently, the encyclopedia of DNA elements (ENCODE) projects revealed the functionality of non-coding sequences comprising various cis-acting elements, chromatin structures, and DNA methylation sites, which open a new era of advanced genetic studies in the addiction field [14]. Understandably, since the brain orchestrates different behaviors through specific neural circuits, the role of genes in these circuits is one of the most important features of addiction research [5,6,13]. Genetic research pursues not only the etiology of addiction, but also the critical need to develop effective treatment methods. For example, a recent study demonstrated that a genetic variant of a mu-opioid receptor appears to determine efficacy of naltrexone in human alcohol-dependents [1]. Addiction and several co-morbid psychiatric disorders share many common neurobiological features. Recent advances in psychiatric studies employing animal models [8] are enabling us to understand the complex nature of addiction at the molecular level. Many efforts are being carried out ","PeriodicalId":90086,"journal":{"name":"Addiction genetics","volume":"1 1","pages":"1 - 2"},"PeriodicalIF":0.0,"publicationDate":"2012-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69088700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}