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Articles by D Goldman
Total Records ( 3 ) for D Goldman
  J. H Barnett , J Heron , D Goldman , P. B Jones and K. Xu
 

OBJECTIVE: Genetic variants that contribute to the risk of psychiatric disorders may also affect normal variation in psychological function. Indeed, the behavioral effects of many genetic variants may be better understood as process-specific rather than disease-specific. A functional valine-to-methionine (Val158Met) polymorphism in the catechol-O-methyltransferase (COMT) gene has been associated with cognitive function and brain metabolic activity accompanying such tasks. Not all studies are consistent, and less is known about the effect of this polymorphism during development. The authors tested the hypothesis that a more informative COMT haplotype predicts normal cognitive development in a large population-based cohort of children enrolled in the Avon Longitudinal Study of Parents and Children. METHOD: Effects on verbal and performance IQ as well as verbal inhibition were assessed at age 8, and effects on working memory were assessed at age 10. From the five COMT single nucleotide polymorphisms (SNPs) genotyped, the effect of a functional three-SNP haplotype consisting of Val158Met and two synonymous SNPs (rs6269 and rs4818), which together exert a major influence on the level of COMT expression and enzyme activity, was evaluated. RESULTS: This three-SNP haplotype predicted both verbal inhibition and working memory, and there was a genotype-by-sex interaction on verbal IQ. The effect of COMT genotype (diplotype) on cognition was curvilinear, which is consistent with the "inverted U" model of dopamine effect on frontal cortical efficiency. In addition, the SNP rs2075507 (previously rs2097603) was independently associated with verbal inhibition, while rs165599 showed no main cognitive effects. However, rs165599 showed a genotype-by-sex interaction with working memory. CONCLUSIONS: Genetic variation at several loci in the COMT gene affects normal cognitive function in children.

  S. G Lindell , M. L Schwandt , H Sun , J. D Sparenborg , K Bjork , J. W Kasckow , W. H Sommer , D Goldman , J. D Higley , S. J Suomi , M Heilig and C. S. Barr
 

Context  Neuropeptide Y (NPY) counters stress and is involved in neuroadaptations that drive escalated alcohol drinking in rodents. In humans, low NPY expression predicts amygdala response and emotional reactivity. Genetic variation that affects the NPY system could moderate stress resilience and susceptibility to alcohol dependence.

Objective  To determine whether functional NPY variation influences behavioral adaptation to stress and alcohol consumption in a nonhuman primate model of early adversity (peer rearing).

Design  We sequenced the rhesus macaque NPY locus (rhNPY) and performed in silico analysis to identify functional variants. We performed gel shift assays using nuclear extract from testes, brain, and hypothalamus. Levels of NPY in cerebrospinal fluid were measured by radioimmunoassay, and messenger RNA levels were assessed in the amygdala using real-time polymerase chain reaction. Animals were exposed to repeated social separation stress and tested for individual differences in alcohol consumption. Animals were genotyped for –1002 T > G, and the data were analyzed using analysis of variance.

Setting  National Institutes of Health Animal Center.

Subjects  Ninety-six rhesus macaques.

Main Outcome Measure  Behavior arousal during social separation stress and ethanol consumption.

Results  The G allele altered binding of regulatory proteins in all nuclear extracts tested, and –1002 T > G resulted in lower levels of NPY expression in the amygdala. Macaques exposed to adversity had lower cerebrospinal fluid NPY levels and exhibited higher levels of arousal during stress, but only as a function of the G allele. We also found that stress-exposed G allele carriers consumed more alcohol and exhibited an escalation in intake over cycles of alcohol availability and deprivation.

Conclusions  Our results suggest a role for NPY promoter variation in the susceptibility to alcohol use disorders and point to NPY as a candidate for examining gene x environment interactions in humans.

 
 
 
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