Dear colleagues,
I am excited to present to you our second issue of 2013 covering latest research results on the identification of genomic biomarkers in schizophrenia as well as new insights into biological underpinnings and pharmacological treatment of pathological gambling.
At the outset of this issue, Leboyer and colleagues reviewed recent studies evidencing an association between human endogenous retrovirus-W (HERV-W) and schizophrenia (SCZ). The authors concluded that a lifelong interaction between infectious agents and HERV-W may decipher the actual development and course of the disease.
On the basis of evidence suggesting RELN to be a risk factor in European populations, Li and colleagues set out to examine its association with SCZ in two independent Han Chinese samples using a case–control association analysis. Their results demonstrate that RELN represents a susceptibility gene for SCZ in Han Chinese ethnicity and likely is a risk gene for the disease in populations worldwide.
In a magnetic resonance imaging (MRI) study, Ohi and colleagues analysed effects of a variant in the AKT1 gene (SNP5; rs2494732), which is associated with SCZ in Asian populations, on memory and attention functions as well as brain structure in a Japanese sample diagnosed with this disease. The findings indicate an association of the polymorphism with attentional deficits and smaller grey matter volume in the right inferior parietal lobule.
Hashimoto and colleagues investigated relationships between a variant in the KCNH2 gene (M30; rs3800779) and multiple SCZ-related cognitive functions in a healthy Japanese sample. Their results suggest an association between the polymorphism and deficits in vigilance and working memory.
Introducing the second thematic focus of this issue, Berlin and colleagues present the first randomized, controlled trial of topiramate in pathological gambling (PG). Treatment effects as measured with questionnaires were found in a self-rating of impulsivity, especially in motor and non-planning subscales.
By using MRI, Yip and colleagues investigated white matter microstructural characteristics in individuals suffering from PG. Together with age and past alcohol abuse or dependence, PG symptoms predicted white matter coherence in the genu of the corpus callosum, thus suggesting a contribution of white matter abnormalities to the pathophysiology of PG.
Because serotonergic mechanisms are known to be involved in substance addictions, Potenza and colleagues set out to analyse their impact in PG by means of ligand-based imaging. The authors provide first evidence that severity of PG is linked to increased levels of 5-HT1B receptors in the ventral striatum, putamen and anterior cingulate cortex.
The issue concludes with a return to the effort of identifying genomic biomarkers in SCZ by a brief report of a case–control study by Li and colleagues. The authors addressed whether or not the FoxP2 gene, which is associated with language disorders, is relevant to SCZ, major depression or bipolar disorder in a Han Chinese sample. Among the 12 analysed SNPs, the authors found significant associations with SCZ and major depression for the genetic variant rs10447760.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor