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In This Issue of JAMA Psychiatry |

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JAMA Psychiatry. 2014;71(10):1091. doi:10.1001/jamapsychiatry.2013.2757.
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Moritz and colleagues examine the 3-year efficacy of metacognitive training for schizophrenia in a 2-center randomized clinical trial. Compared with neuropsychological training, the metacognitive training group demonstrated significantly greater reductions in the Positive and Negative Syndrome Scale delusion and positive syndrome scores, as well as in the Psychotic Symptom Rating Scales delusion score. Improvements in self-esteem and quality of life favoring metacognitive training were also found, which did not distinguish groups at previous assessment points (“sleeper” effects).

ZNF804A is a leading gene associated with schizophrenia risk, but the biological basis for its involvement is unknown. In this issue, Tao and colleagues identified a novel, shorter variant of ZNF804A and showed that it may be a mediator of the genetic association. The effect was only seen in the fetal brain, extending the evidence that the prenatal period is a critical time for genetic mechanisms underlying schizophrenia. The specific functions of the ZNF804A variant remain unknown.

Bernert and colleagues evaluate poor subjective sleep quality and the risk for late-life suicide within a multisite population-based study. Based on a longitudinal investigation of 14 456 older adults in the Established Populations for Epidemiologic Studies of the Elderly, poor sleep quality conferred elevated risk for death by suicide 10 years later, independent of depressed mood.

In this randomized clinical trial by Hollon and colleagues, 452 patients with major depression are treated for as long as 3 years with antidepressant medications or augmenting agents necessary to bring them to recovery. Half of the patients also received cognitive therapy. The recovery rate was higher in combined treatment, especially among patients with severe, nonchronic depression. The combination was not required for patients with less severe depression and those with chronic depression did not benefit.

Genetic risk factors have been implicated in posttraumatic stress disorder (PTSD) vulnerability. Using an Ohio National Guard cohort and replicating it in an independent Grady Trauma Project cohort, Liberzon and colleagues identified a novel association of a single-nucleotide polymorphism in the promoter region of the ADRB2 gene with PTSD symptoms in interaction with childhood trauma. This ADRB2 polymorphism has been linked to adrenergic system function.




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