Moffitt et alArticle summarize emerging evidence for gene-environment interaction (GxE) in psychiatry. They argue that GxE research should be hypothesis driven and describe 7 strategic steps for future studies. They suggest that ignoring nurture handicaps the field’s capacity to make new discoveries about nature. The GxE strategies may benefit gene hunters.
A computational model by Talamini et alArticle provides novel insights into the contributions of hippocampal and parahippocampal regions to memory processing in schizophrenia. The model plausibly simulates performance of healthy subjects on several episodic memory tasks. Schizophrenia-like memory deficits emerge when “cortical” and “entorhinal” inputs to the “hippocampus” are reduced but not when noise is increased or hippocampal units (“neurons”) are destroyed. Thus, abnormal medial temporal lobe connectivity may underlie the persistent memory deficits in schizophrenia.
Butler et alArticle examined early-stage visual pathway dysfunction in schizophrenia using electrophysiology, psychophysics, and diffusion tensor imaging. Deficits particularly involving the magnocellular visual pathway were found. This study provides evidence that early-stage visual processing deficits are related to decreased nonlinear signal amplification. Diffusion tensor imaging studies support the hypothesis of dysfunction within low-level visual pathways involving thalamocortical radiations. Deficits in early-stage visual processing significantly predicted higher cognitive deficits.
Using data from a 7-site, randomized “implementation effectiveness” trial of evidence-based supported employment, Cook et alArticle found that experimental-condition subjects with severe mental illness were more likely than comparison subjects to be competitively employed, work 40 or more hours in a month, and have higher earnings, despite controlling for demographic, clinical, work history, disability beneficiary status, and study site confounds.
Schatzberg et alArticle investigated switching chronically depressed nonresponders treated with nefazodone or cognitive behavioral analysis stem of psychotherapy (CBASP) to the alternate monotherapy. While there were no significant differences in the response rates among completers, in the intent-to-treat analysis, a higher response rate was observed among those switched from nefazodone to CBASP (57.4%) than vice versa (42.1%). A switch from medication to psychotherapy or vice versa may be useful for nonresponders.
To identify patients with mild traumatic brain injury (MTBI) at risk for major depressive episode, Levin et alArticle administered the Center for Epidemiologic Studies Depression Scale to 130 patients with MTBI at 1 week after injury and the depressive episode module of the Structured Clinical Interview for DSM-IV at 3 months’ postinjury. A prediction model using the receiver operating characteristic curve supported the feasibility of early identification of patients with MTBI at high risk for a major depressive episode.
While genetic effects apparently modify the depressogenic effects of stressful life events (SLEs), it is not clear which specific genes are involved. Kendler et alArticle attempt to replicate prior findings suggesting that a functional variant in the serotonin transporter (5-HTT) might explain these findings. Individuals with 2 short alleles (ss) at the 5-HTT locus were more sensitive to the depressogenic effects of SLEs than were those with 1 or 2 long alleles, and this resulted almost entirely from an increased sensitivity of SS individuals to the depressogenic effects of common low-threat events. These results suggest that variation at the 5-HTT moderates the sensitivity of individuals to the depressogenic effects of mild to moderate SLEs
Taylor et alArticle examined the influence of polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR) on hippocampal volumes in 72 elderly subjects with early-onset depression, 63 elderly subjects with late-onset depression, and 83 healthy elderly control subjects. Subjects with late-onset depression with the L/L genotype had significantly smaller right hippocampal volumes than did either subjects with early-onset depression or control subjects.
Children exposed to a traumatic event may be at higher risk for developing mental disorders. Using a sample of 8236 randomly selected New York City public school students (grades 4-12) 6 months after September 11, 2001, Hoven et alArticle projected 205 000 students had 1 or more of 6 probable anxiety/depressive disorders. Continued exposure to stress from ongoing terrorist threats and exposure to community violence has the potential to increase 9/11-related psychopathology among children in New York City.
Using data from the Project on Human Development in Chicago Neighborhoods, Xue et alArticle examined associations among children’s mental health and neighborhood economic and social conditions in a sample of children aged 5 to 11 years. A public health concern is the large number of children in disadvantaged neighborhoods with mental health problems. The mechanism through which neighborhood economic effects operated was collective efficacy, which may be amenable to intervention.
Silverman et alArticle examine the familial aggregation of Alzheimer disease (AD) and the relationship between age at onset and the familial/genetic factors associated with AD across the late life span. The results have implications both on the varying role of genetic risk factors in AD at different ages and for estimating the risk of illness for first-degree relatives of patients with AD.
This Month in Archives of General Psychiatry. Arch Gen Psychiatry. 2005;62(5):468. doi:10.1001/archpsyc.62.5.468