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Owen et al reviewed recent genome-wide studies of schizophrenia and bipolar disorder. There are strongly supported associations with common alleles for both disorders and in the case of schizophrenia, clear evidence for involvement of copy number variants. Robust findings are still few in number and cumulatively account for a small amount of the population variance in risk. Nevertheless, they represent a step change in that they clearly indicate the tractability of these disorders to genomic approaches.
Eack et al used structural magnetic resonance imaging to examine gray matter change in patients with early-course schizophrenia treated for 2 years with either cognitive enhancement therapy or an enriched supportive therapy control. They found that patients treated with cognitive enhancement therapy demonstrated greater preservation of gray matter in left medial-temporal brain regions, as well as gray matter increases in the left amygdala, which were associated with improved social and nonsocial cognition.
Fusar-Poli et al combined functional magnetic resonance imaging during a working memory task and fluorine 18–labeled fluorodopa positron emission tomography to investigate the relationship between striatal dopamine activity and prefrontal function in people at ultra high risk of psychosis. A direct relationship between altered prefrontal cortical function and subcortical changes in dopamine activity was observed, consistent with the notion that frontostriatal interactions play a critical role in the pathoetiology of psychosis.
Walters et al examined the effects on cognition of the ZNF804A variant rs6490121, identified as a genome-wide significant risk variant for psychosis. The risk genotype was found to be associated with significant difference in both episodic memory and working memory in cases but not controls in independent Irish and German samples. Contrary to expectations, risk patient carriers showed relatively intact memory performance compared with nonrisk carriers.
Whether obsessive-compulsive disorder (OCD) is adequately classified as an anxiety disorder is a matter of considerable debate. Radua et al used novel voxel-based meta-analytic methods to compare brain gray matter volumes across several anxiety disorders. They found common (reduced volume in dorsomedial frontal/anterior cingulate gyri) as well as distinct (increased basal ganglia volume in OCD vs decreased volume in other anxiety disorders) neural substrates in OCD vs other anxiety disorders.
Using data from a nationally representative community mental health survey linked with national child protection agency records, Scott et al found that child protection agency history was associated with a range of subsequent DSM-IV mental disorders in young adults. These associations increased in magnitude when those retrospectively reporting child maltreatment were removed from the comparison group.
Sourander et al examined psychosocial and psychiatric risk factors associated with cyberbullying among 2215 Finnish adolescents. Altogether, 5% were only cybervictims; 7%, only cyberbullies; and 5%, both cyberbullies and cybervictims. Both cyberbullying and cybervictimization were associated with psychiatric and psychosomatic problems. The most troubled were those who were both cyberbullies and cybervictims. There is a need for new strategies for cyberbullying prevention and intervention.
Using functional neuroimaging, Passamonti et al explored the response to emotional and neutral faces in early- and adolescence-onset conduct disorder. Contrary to the developmental taxonomic theory that posits that only early-onset conduct disorder has a neurodevelopmental basis, both conduct disorder subtypes showed an abnormal response in brain regions thought to underlie antisocial behavior. Additional amygdala hypofunction in response to sad faces in early-onset conduct disorder alone may reflect the more severe and persistent nature of this subtype.
Thambisetty et al performed a proteomics study of plasma in Alzheimer disease finding clusterin concentration to be associated with faster cognitive decline and greater brain atrophy. They replicated this finding and also showed an increase in plasma clusterin concentration in association with amyloid pathology in man using carbon 11–labeled Pittsburgh Compound B positron emission tomography imaging as well as in a transgenic mouse model. These results add weight to recent genome-wide studies associating clusterin with disease susceptibility.
In a prospective cohort study of more than 1000 outpatients with stable coronary heart disease, Martens et al found a strong and robust association between generalized anxiety disorder and cardiovascular events. Patients with anxiety disorder had a 74% greater rate of subsequent cardiovascular events. This association was not explained by differences in cardiac disease severity, depressive disorder, biological mediators, or health behaviors.
This Month in Archives of General Psychiatry. Arch Gen Psychiatry. 2010;67(7):665. doi:10.1001/archgenpsychiatry.2010.72
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