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In This Issue of JAMA Psychiatry |

In This Issue of JAMA Psychiatry FREE

JAMA Psychiatry. 2013;70(1):5. doi:10.1001/jamapsychiatry.2013.815.
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Kubota et alArticle conducted a magnetic resonance imaging study to investigate the association between thalamocortical disconnection and cortical thinning in schizophrenia in vivo. Schizophrenic patients had reduced fractional anisotropy in the right thalamo-orbitofrontal pathway. Fractional anisotropy for this pathway was correlated with cortical thinning of the right frontal polar and lateral orbitofrontal regions in the patients.

Power et alArticle examined the reproductive fitness of individuals with psychiatric disorders and their healthy siblings compared with the general population. Affected men showed a consistently greater reduction in number of children compared with women. Unaffected siblings often had a significantly greater number of children than the general population.

In a randomized clinical trial, Raison et alArticle examined the efficacy of the tumor necrosis factor antagonist infliximab in patients with treatment-resistant depression. Infliximab did not exhibit a generalized antidepressant effect. However, in patients with evidence of increased peripheral inflammation, infliximab led to a greater decrease in depressive symptoms than placebo. These data suggest that increased peripheral inflammatory biomarkers identify depressed patients who may be uniquely responsive to immune-targeted therapy.

Georgiades et alArticle prospectively examined the emergence of autistic-like traits in infant siblings of probands diagnosed with autism spectrum disorder who themselves were not diagnosed with autism spectrum disorder at age 3 years. Study findings suggest that autistic-like traits resembling a “broader autism phenotype” emerge by 12 months of age in 19% of these unaffected siblings.

Suzuki et alArticle examined microglial activation by positron emission tomography and found significantly augmented activation of microglia in multiple brain regions of young adults with autism spectrum disorder as compared with controls. The finding supports the idea that microglial activation might play a role in the pathogenesis of the disorder.

Ecker et alArticle investigated differences in surface area (SA) and thickness (CT) of the cortex in a large, well-characterized sample of men with autism spectrum disorder. The spatially distributed patterns of differences in SA and CT were largely nonoverlapping, suggesting that regional variations in cortical volume in autism spectrum disorder may be underpinned by independent variations in SA and CT, which most likely represent separable neurobiological mechanisms.

Volk et alArticle examined the association between exposure to air pollutants and autism risk in 279 autism cases and 245 typically developing controls from the Childhood Autism Risks From Genetics and the Environment study. Their findings showed that cases were more likely to have lived at residences with higher air pollution exposure from traffic and regional sources during pregnancy and the first year of life.

Kendler et alArticle examined the genetic and environmental dimensions underlying DSM criteria for conduct disorder in a large twin sample. From a genetic perspective, these criteria do not reflect a single dimension of liability. The familial risk to conduct disorder has 2 dimensions of genetic risk, reflecting rule breaking and overt aggression, and 1 dimension of shared environmental risk, reflecting covert delinquency. These familial factors differ in their association with a range of relevant validators.

Doehrmann et alArticle collected pretreatment functional magnetic resonance imaging data for predicting the outcome of subsequent cognitive behavioral therapy in patients with social anxiety disorder. Using analytical techniques that support generalization of the results, they found that combining brain measures with information on initial clinical severity accounted for more than 40% of the variance in treatment response and substantially exceeded predictions based on clinical measures alone.

Haghighi et alArticle examined the associations between prenatal exposure to maternal cigarette smoking and offspring fat intake, risk for obesity, and structural variations in brain regions involved in reward processing in a cohort of 378 adolescents. The results suggest that prenatal exposure to maternal cigarette smoking may promote obesity by enhancing dietary preference for fat and that this effect may be mediated in part through subtle structural variations in the amygdala.

Fusar-Poli et alArticle present a consensus review addressing the progress in the field of prodromal psychosis made over the past decade. This article defines the historical, diagnostic, prognostic, psychopathological, therapeutic, and neurobiological advances made as well as recognizes substantial limitations. This critical review sets the stage for future investigations of subjects at high clinical risk for psychosis.

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