In this issue, Goldman et al (SEE ARTICLE) used a high-throughput technique to map cortical thickness in 196 normal controls, 115 affected patients with schizophrenia, and 192 unaffected siblings to study disease-related heritability. The data show widespread thickness reductions in the patient group, most pronouncedly in the frontal lobe and temporal cortex, but only trend-level reductions in siblings. Analysis of heritability of these changes (using the Risch 
measure) revealed widespread evidence for heritability for cortical thickness.
In a combined functional and spectroscopical brain imaging study, Walter et al (SEE ARTICLE) investigated the molecular basis of altered brain responses in major depression. Reduced signal changes in the pregenual portion of the anterior cingulate gyrus, especially in patients with highly anhedonic major depressive disorder, correlated significantly with generally lower glutamine levels and decreased emotional intensity during affective picture viewing as compared with healthy controls.
Licinio et al (SEE ARTICLE) resequenced the brain-derived neurotrophic factor gene (BDNF) in 264 controls and 272 depressed Mexican Americans; 83 novel single-nucleotide polymorphisms (SNPs) were identified, in the context of 254 BNDF SNPs known to date. One SNP (rs12273539) and 2 haplotypes remained significant for association with major depression and 1 novel 5' untranslated region SNP was associated with antidepressant response.
Linke et al (SEE ARTICLE) used principal components analysis and Cox regression survival models to examine the relationships among depressive symptom dimensions and cardiovascular outcomes, including heart failure, myocardial infarction, stroke, and cardiovascular-related death, in a sample of 550 women with suspected myocardial ischemia tracked for a median of 5.8 years. Results showed that somatic but not cognitive/affective depressive symptoms were associated with worse cardiovascular prognosis.
Examining a longitudinal sample, Mosconi et al (SEE ARTICLE) detected enlarged amygdala volume by 2 years of age in children with autism. Enlargement was associated with joint attention ability, supporting evidence that the amygdala is structurally abnormal in autism and that alterations to this structure may be linked to a core deficit of this disorder.
Losh et al (SEE ARTICLE) investigated the neuropsychological profiles of autism and the broad autism phenotype (ie, constellation of language, personality, and social-behavioral features present among relatives that mirror the symptom domains of autism but are much milder in expression). They found parallel patterns of performance in autism and relatives that suggest the domain of social cognition may be an important target for linking phenotype to cognitive process to brain structure in autism.
In a large longitudinal population-based study, Schreier et al (SEE ARTICLE) found that peer victimization in childhood, especially if chronic or severe, increased the risk for psychotic symptoms in early adolescence. These results lend further support to the relevance of psychosocial factors in the etiology of psychotic symptoms in nonclinical populations.
Freeman et al (SEE ARTICLE) compared the rates of relapse and time to relapse between short-term and long-term sertraline hydrochloride treatment of women diagnosed with premenstrual syndrome or premenstrual dysphoric disorder. The relapse rate was significantly higher and the time to relapse was shorter after short-term treatment compared with long-term treatment. Subjects with severe baseline symptoms were more likely to relapse compared with the low to moderate group and were more likely to relapse with short-term treatment.
In a population-based magnetic resonance imaging study, Vernooij et al (SEE ARTICLE) examined how brain white matter microstructure relates to cognition in elderly persons. Microstructural integrity as assessed with diffusion tensor imaging of both white matter lesions and normal-appearing white matter was associated with cognition, regardless of white matter atrophy and white matter lesion volume.
Fallon et al (SEE ARTICLE) examined brain blood flow and metabolism among 35 patients with persistent Lyme encephalopathy and 17 matched healthy volunteers. While global differences were not seen, regional abnormalities in flow and metabolism were found consistently in particular areas across all measurement conditions, primarily reflecting hypoactivity. Close coupling between flow and metabolism suggests these abnormalities are metabolically driven.
