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Biomedical subjects

Wade Berrettini

Publications and source records attributed to Wade Berrettini.

5 recordsLinked to original sources
PubMed2003

A functional polymorphism of the mu-opioid receptor gene is associated with naltrexone response in alcohol-dependent patients.

This study examined the association between two specific polymorphisms of the gene encoding the mu-opioid receptor and treatment outcomes in alcohol-dependent patients who were prescribed naltrexone or placebo. A total of 82 patients (71 of European descent) who were randomized to naltrexone and 59 who were randomized to placebo (all of European descent) in one of three randomized, placebo-controlled clinical trials of naltrexone were genotyped at the A(+118)G (Asn40Asp) and C(+17)T (Ala6Val) SNPs in the gene encoding the mu-opioid receptor (OPRM1). The association between genotype and drinking outcomes was measured over 12 weeks of treatment. In subjects of European descent, individuals with one or two copies of the Asp40 allele treated with naltrexone had significantly lower rates of relapse (p=0.044) and a longer time to return to heavy drinking (p=0.040) than those homozygous for the Asn40 allele. There were no differences in overall abstinence rates (p=0.611), nor were there differences in relapse rates or abstinence rates between the two genotype groups among those assigned to placebo. These preliminary results are consistent with prior literature demonstrating that the opioid system is involved in the reinforcing properties of alcohol and that allelic variation at OPRM1 is associated with differential response to a mu-receptor antagonist. If replicated, these results would help to identify alcohol-dependent individuals who may be most likely to respond to treatment with naltrexone.

Adult↗
PubMed2003

Genomewide linkage analyses of bipolar disorder: a new sample of 250 pedigrees from the National Institute of Mental Health Genetics Initiative.

We conducted genomewide linkage analyses on 1,152 individuals from 250 families segregating for bipolar disorder and related affective illnesses. These pedigrees were ascertained at 10 sites in the United States, through a proband with bipolar I affective disorder and a sibling with bipolar I or schizoaffective disorder, bipolar type. Uniform methods of ascertainment and assessment were used at all sites. A 9-cM screen was performed by use of 391 markers, with an average heterozygosity of 0.76. Multipoint, nonparametric linkage analyses were conducted in affected relative pairs. Additionally, simulation analyses were performed to determine genomewide significance levels for this study. Three hierarchical models of affection were analyzed. Significant evidence for linkage (genomewide P<.05) was found on chromosome 17q, with a peak maximum LOD score of 3.63, at the marker D17S928, and on chromosome 6q, with a peak maximum LOD score of 3.61, near the marker D6S1021. These loci met both standard and simulation-based criteria for genomewide significance. Suggestive evidence of linkage was observed in three other regions (genomewide P<.10), on chromosomes 2p, 3q, and 8q. This study, which is based on the largest linkage sample for bipolar disorder analyzed to date, indicates that several genes contribute to bipolar disorder.

Bipolar Disorder↗
PubMed2003

Elucidating the role of genetic factors in smoking behavior and nicotine dependence.

Despite over a decade of intensive tobacco control efforts, a substantial proportion of the world's population continues to smoke. With advances in molecular biology and genomics technology, attention is focusing on the genetic basis of addiction to nicotine. The hope is that by better understanding the biology of nicotine addiction, novel prevention and cessation strategies can be developed and targeted to individuals most likely to benefit. This article provides an overview of currently available data from genetics research on smoking behavior and discusses study design issues to be addressed to make progress in this line of research.

Animals↗
PubMed2002

Review of bipolar molecular linkage and association studies.

This paper reviews the history of molecular genetic linkage and linkage disequilibrium (LD) or association studies of bipolar disorder (BPD). The topic is introduced with a brief discussion of various genetic concepts, including linkage and linkage disequilibrium. It is emphasized that criteria for declaring linkage must include independent confirmation by multiple groups of investigators. Given that the inherited susceptibility for BPD is most likely explained by multiple genes of small effect, simulations indicate that universal confirmation of valid linkages cannot be expected due to sampling variation and genetic heterogeneity. With this background, several valid linkages of BPD to genomic regions are reviewed, including some which may be shared with schizophrenia. These results suggest that nosology must be changed to reflect the genetic origins of the multiple disorders which are collectively described by the term, BPD. The history of BPD LD studies is reviewed, using monoamine oxidase as as an example. Some suggestions of improving these BPD LD are offered.

Bipolar Disorder↗