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From a large multisite study, Anton et al (page 135) found that a genetic variant of the μ-opiate receptor was associated with naltrexone hydrochloride efficacy. Individuals having at least 1 copy of the Asp40 coding allele and who received naltrexone and medical management had better outcomes than those with the more common Asn40/Asn40 genotype.
Khashan et al (page 146) investigated the association between antenatal maternal exposure to an objective measure of stress and risk of schizophrenia in the offspring using data from the Danish National Register (N = 1.3 million). The results showed a 70% increase in risk of schizophrenia among offspring of mothers who were exposed to severe stress in the first trimester.
Deakin et al (page 154) used functional magnetic resonance imaging to examine neural activity during intravenous ketamine infusion. They found a striking pattern of inhibited regions in the ventral frontotemporal cortex, which correlated with dissociative experiences, while activations in the posterior cingulate correlated with psychosis ratings. The glutamate release inhibitor lamotrigine blocked most of the effects. The results suggest that N-methyl-D-aspartate hypofunction results in increased glutamate release, which may mediate aspects of psychosis.
Mittal et al (page 165) examined longitudinal progression of movement abnormalities in adolescents at risk for developing schizophrenia. High-risk adolescents exhibited elevated frequency and showed significant movement abnormality increase over time in comparison with clinical and nonclinical controls. The magnitude of relationship between symptoms and movement abnormalities increased throughout the course of the prodromal period.
Barry et al (page 172) evaluated the association between sex and the likelihood of 6 possible transitions, namely, from nondepressed or depressed to nondepressed, depressed, or death, at 18-month intervals over 72 months among persons 70 years and older. Among older persons, the higher burden of depression in women than men appears to be attributable to a greater susceptibility to depression and, once depressed, to more persistent depression and a lower probability of death.
Holmes and Pizzagalli (page 179) found that unmedicated subjects with depression showed behavioral and electrophysiological markers indicating dysfunctions in the automatic detection of error commission. These impairments were accompanied by paralimbic hyperactivation (rostral anterior cingulate cortex) 80 milliseconds after committing an error and a subsequent failure to recruit prefrontal regions critically implicated in cognitive control.
Genetic inheritance and developmental life stress both contribute to major depressive disorder in adults. Bradley et al (page 190) report an association study examining gene × environment interactions between genetic polymorphisms at the corticotropin-releasing hormone type 1 receptor (CRHR1) locus and measures of child abuse on depressive symptoms. These data support the corticotropin-releasing hormone hypothesis of depression and suggest that CRHR1 genotype moderates the effect of child abuse on adult depression.
Caspi et al (page 203) tested if variations in the catechol O-methyltransferase gene (COMT) would help to identify children with attention-deficit/hyperactivity disorder who exhibit antisocial behavior. The COMT Val158Met variant was associated with phenotypic variations among children with attention-deficit/hyperactivity disorder. Across 3 samples, valine/valine homozygotes had more symptoms of conduct disorder, more aggression, and greater risk of criminal offending.
Ouellet-Morin et al (page 211) examined the genetic and environmental contributions to cortisol reactivity in unfamiliar situations as a function of familial adversity (FA) among 19-month-old twins. Genetic factors accounted for cortisol reactivity under low FA but not under high FA, where cortisol reactivity was associated with shared and unique environment. Familial adversity may have an early programming developmental effect on cortisol reactivity.
Scott et al (page 220) examined the response of 2 neuronal systems, dopaminergic and opioid, with molecular imaging techniques, while healthy individuals were administered a placebo with possible analgesic properties. Placebo administration was associated with enhancements or reductions in the release of dopamine and endogenous opioids in a manner proportional to individual expectations, as well as the improvement or worsening of experimental pain ratings.
This Month in Archives of General Psychiatry. Arch Gen Psychiatry. 2008;65(2):129. doi:10.1001/archgenpsychiatry.2007.28