Dear colleagues,
I am delighted to introduce to you the third issue of 2015 featuring the updated third part of the WFSBP Guidelines for Biological Treatment of Schizophrenia and original research on biological markers and cognitive characteristics in schizophrenia and impulse control disorders.
The WFSBP Guidelines for Biological Treatment of Schizophrenia, Part 3: Management of special circumstances represent an evidence-based update of the first edition of WFSBP Schizophrenia Guidelines published in the years 2005 and 2006. They cover the management of specific treatment circumstances: comorbid depression, suicidality, various comorbid substance use disorders (legal and illegal drugs) and pregnancy and lactation. Based on a systematic review and evaluation of up-to-date literature, this comprehensive manual provides clinically and scientifically relevant practice recommendations. These may be used world-wide by physicians treating patients with schizophrenia (SCZ) in order to further improve therapy progress, effectiveness and outcomes. My sincere gratitude is expressed to Alkomiet Hasan and to the entire WFSBP Task Force on Treatment Guidelines for Schizophrenia for their magnificent work.
Zai and colleagues set out to investigate the role of brain-derived neurotrophic factor (BDNF) and DRD3 genes in suicidal behaviour in SCZ. The authors indeed found a possible role of the BDNF Val66Met and DRD3 Ser9Gly SNPs in increasing the risk of suicide attempts in 188 SCZ patients. Specifically, a larger proportion of SCZ patients who were carrying at least one copy of the minor allele at each of the Val66Met and Ser9Gly functional markers had attempted suicides compared to patients with other genotypes.
Introducing our second topic, Schwarz and co-workers examined the impact of methylphenidate (MPH) on gene expression levels of lymphoblastoid cells derived from adult ADHD patients and healthy controls by hypothesis-free, genome-wide microarray analysis. Results revealed chronic MPH treatment effects on the expression of ATXN1, HEY1, MAP3K8 and GLUT3 in controls as well as acute treatment effects on the expression of NAV2 and ATXN1 specifically in ADHD patients.
Using voxel-based morphometry, Villemonteix and colleagues investigated the effects of Val158Met polymorphism on grey matter volumes in children with ADHD and healthy controls. Compared to the latter, ADHD children had decreased grey matter volume in the inferior frontal gyrus (IFG). Volume in this region was negatively correlated with ratings of hyperactivity/impulsivity symptoms. In addition, only children carrying the Met158 allele exhibited such a decrease in the IFG. Children with ADHD homocygotes for the Val158 allele presented increased grey matter volume in the caudate nucleus, when compared to controls.
Ivanova and co-workers explored a possible association between tardive dyskinesia (TD) and CYP1A2 polymorphism in 319 psychiatric inpatients and 117 healthy controls. Results revealed that limb-truncal, but not oro-facial TD was associated with CYP1A2 polymorphism and that patients with the C/C genotype had a higher symptom load than those with the A/C or the A/A genotype.
Finally, a brief report by Wichniak and colleagues presents results on an association between electroencephalographic (EEG) spectral power and a wide range of cognitive functions measured with the MATRICS Consensus Cognitive Battery (MCCB) in SCZ patients. The authors found that superior cognitive performance was associated with less power of theta waves. Six MCCB cognitive tests showed correlations with absolute theta power and three tests with relative theta power, with increased theta power being linked especially to memory deficits.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor