In This Issue

Two studies highlight potentially remediable aspects of schizophrenia that interfere with social functioning. Hoptman et al. (CME, p. 939) pinpoint urgency—rash action driven by strong emotion—as the type of impulsivity underlying aggression in schizophrenia patients. Urgency can be fueled by either positive or negative emotion and correlates with general symptoms, such as anxiety. It is associated with brain regions mediating response inhibition and conflict monitoring, notes Szeszko in an editorial (p. 897). The severe reading deficits (figure) of schizophrenia patients tested by Revheim et al. (p. 949) were due to both visuospatial and phonological impairment, but not overall cognitive dysfunction. Reading impairment did not appear to reflect poor premorbid reading ability.

Pregnant Finnish women with high levels of C-reactive protein, a marker of inflammation, were more likely to have offspring who developed schizophrenia by early adulthood. Canetta et al. (CME, p. 960) compared archived maternal blood serum specimens for 777 schizophrenia patients and control subjects. The connection between inflammation and stress, state Cannon et al. in an editorial, (p. 901), indicates that psychiatrists need to be involved to help pregnant women manage stress, anxiety, and depression, to protect both mother and child.

Schizophrenia’s cognitive deficits appear to involve low levels of GAD67, a key enzyme for synthesizing the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Expression of the GAD67 gene can be regulated by the transcription factor Zif268, and Kimoto et al. (p. 969) found that both GAD67 and Zif268 mRNA levels were low, and correlated, in brains of schizophrenia subjects. Paterson et al. (p. 979) demonstrated that several neuregulin 1 (NRG1) molecules show patterns of temporal regulation consistent with a role in developmental abnormalities in early childhood. A single-nucleotide polymorphism (SNP) in one of the molecular variants has already been implicated in impaired neurocognition and sensory processing in schizophrenia. Editorialist Sohal (p. 906) points out the increasing convergence between the molecular evidence for genetic risk and the physiological evidence for decreased inhibitory function in schizophrenia.