In This Issue

Imaging studies of brain functioning during cognitive testing exposed key aberrations in the cingulate gyrus of patients with three psychiatric disorders. Etkin and Schatzberg (CME, p. 968) observed processing deficits in the ventral anterior cingulate and amygdala of patients with major depression and/or generalized anxiety disorder, but those with depression only had compensatory prefrontal activity. The twin study by Shin et al. (CME, p. 979) suggests genetic vulnerability to posttraumatic stress disorder (PTSD). Not only did combat veterans with PTSD show greater activation of the dorsal anterior cingulate than combat veterans without PTSD, but so did their monozygotic co-twins without combat exposure. The editorial by Pine and Freedman (p. 885) describes how animal models based on the functions of these neural circuits during fear conditioning could facilitate development of new treatments for human mental disorders.

The prevalence of autism spectrum disorders was 2.6% in South Korean children ages 7–12. Kim et al. (p. 904) attribute the high rate to rigorous screening of both a population sample and children known to have special needs. Many of the diagnosed children were attending regular schools. The editorial by Charman (p. 873) identifies several reasons for variation in autism prevalence among studies.

Genes affecting glutamate neurotransmission featured prominently in associations between 94 genes and 12 inherited physiological or cognitive characteristics of schizophrenia. Greenwood et al. (p. 930) examined 1,536 single-nucleotide polymorphisms (SNPs) in multiple members of 130 families of people with schizophrenia. Each subject also completed tests of attention, memory, abstraction, response inhibition, and emotion recognition. Of 16,620 possible SNP-trait associations, 47 showed strong significance. In his editorial, Goldman (p. 879) notes that genetic findings on schizophrenia appear to converge on the dysfunction of brain circuits.