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lu et al (SEE ARTICLE) compared various forms of ill treatment and physical torture during captivity in terms of their psychological impact in 279 survivors of torture in former Yugoslavia. Psychological manipulations, humiliating treatment, exposure to aversive environmental conditions, and forced stress positions showed considerable overlap with physical torture stressors in terms of associated distress. They were also as likely to lead to posttraumatic stress disorder and depression as physical torture.
Heinks-Maldonado et al (SEE ARTICLE) assessed the forward model in schizophrenia using the N100 component of the auditory event-related potential to altered or unaltered speech. Hallucinating patients did not show suppression of N100 to unaltered self-voice feedback relative to altered voice feedback, suggesting imprecision of this mechanism.
In a meta-analysis including 1065 independent first-degree relatives of patients with schizophrenia and 1100 comparison subjects, Boos et al (SEE ARTICLE) show that relatives have smaller hippocampal and gray matter volumes and larger third ventricle volumes as compared with healthy control subjects. These brain abnormalities found in relatives are similar to the areas that are affected in patients with schizophrenia, but less pronounced.
Using data from the National Survey of American Life, Williams et al (SEE ARTICLE) show that the risk of major depressive disorder (MDD) is similar for Caribbean blacks and African Americans but both black groups have a lower lifetime risk of MDD than whites. However, for both black groups, MDD is more severely disabling and persistent in course than for whites. Moreover, only 45% of African Americans and 24% of Caribbean blacks with MDD in the past year had received any treatment.
Wray et al (SEE ARTICLE) report a genetic association between variants of the gene encoding plexin A2 and anxiety disorders. Plexins are receptors for semaphorins, which together have been implicated in the development of the nervous system but also in neurogenesis within the adult brain. Given the comorbidity between depression and anxiety disorders, the results could provide support for the adult neurogenesis theory of depression.
Dunlop and Nemeroff (SEE ARTICLE) review the evidence for alterations in dopamine circuits in the pathophysiology of major depression. Reductions of motivation, concentration, and pleasure in depression may be mediated by dopaminergic dysregulation, as suggested by findings from animal models, postmortem and neuroimaging studies, and clinical trials of dopaminergic agents. Enhancing dopaminergic transmission should be a focus of new antidepressant drug development.
In a longitudinal community-based study, girls with low birth weight (<2500 g) were 5 to 8 times as likely to have depressive disorders during adolescence as normal-birth-weight girls or boys at any age. Costello et al (SEE ARTICLE) found that after controlling for perinatal, childhood, and adolescent risk, low birth weight continued to predict depression, supporting the fetal programming hypothesis.
Webb et al (SEE ARTICLE) investigated cause-specific mortality in Danish children and young adults whose parents had been admitted for psychiatric treatment. They found significantly higher risks of unnatural-cause mortality. The highest relative risks found were for child homicide. Risks of suicide and open-verdict death were elevated in young adults, markedly so if both parents were previously admitted for psychiatric treatment and if such deaths occurred by poisoning.
Jokela et al (SEE ARTICLE) found a gene x environment interaction involving the serotonin receptor 2A (HTR2A) gene, maternal nurturance, and depressive symptoms in a population-based sample. Exposure to high maternal nurturance in childhood or adolescence predicted low depressive symptoms in adulthood in individuals carrying the T/T or T/C genotype of the T102C polymorphism, but not in individuals carrying the C/C genotype.
Using a twin design, Kremen et al (SEE ARTICLE) showed that cognitive ability assessed prior to trauma exposure predicts risk for posttraumatic stress disorder (PTSD). Risk of developing PTSD was 48% lower in the highest compared with the lowest cognitive ability quartile. In PTSD-discordant pairs, twins with PTSD had lower preexposure cognitive ability than their co-twins. Genetic influences on preexposure cognitive ability explained 5% of the variation in PTSD.
It has been proposed that a µ-opioid receptor gene variant (OPRM118G) increases pleasurable actions of alcohol, risk for alcohol dependence, and therapeutic response to naltrexone. Barr et al (SEE ARTICLE) report that, in rhesus macaques, a functionally equivalent polymorphism (OPRM177G) is associated with increased alcohol-induced stimulation, alcohol preference, and consumption in males. This strongly supports the notion that genetic variation at the µ-opioid receptor locus modulates alcohol reward, primarily among males.
