Dear colleagues,
It is my great pleasure to introduce to you the third issue of 2017 featuring the second part of the WFSBP Consensus Statement on biological markers in anxiety disorders as well as original research on treatment options in anxiety disorders and biomarkers in schizophrenia.
The WFSBP Consensus reviews the current literature on the neurochemistry, neurophysiology and neurocognition in anxiety disorders, obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD). After discussing various biomarkers in relation to anxiety disorders the authors conclude that none of the present biomarkers is sufficient and specific as a diagnostic tool although there is an abundance of research that should improve our understanding of the neurobiological causes of anxiety disorders, OCD and PTSD.
Coleman and colleagues examined the effects of genetic variants on treatment response of exposure-based cognitive behavioural therapy (eCBT) for anxiety disorders. They did not find any associations and genetic variants did not significantly predict treatment response alone or in polygenic risk scores. They conclude that further studies with larger sample sizes are needed in order to detect any associations.
Using voxel-based morphometry, Riederer et al. investigated nondermatomal somatosensory deficits (NDSDs) in relation to cerebral grey matter changes in the sensory system and pain processing regions. They did indeed detect grey matter changes in sensory and temporal cortices, thalamus and the hippocampus/fusiform gyrus. They also found that anxiety scores were higher in NDSDs patients and that anxiety correlated negatively with grey matter in the frontal cortex.
Ivanova and associates aimed to identify 5-HT genetic variants modulating hyperprolactinaemia (HPRL) in antipsychotic treated patients with schizophrenia. Results revealed an association between HPRL and X-chromosome haplotypes of the SNPs rs569959 and rs17326429 while no association between the autosomal markers was detected.
In a brief report, Bortolato and colleagues investigated the effect of catechol-O-methyltransferase (COMT) catalytic activity in post-mortem brain tissue of patients with bipolar disorder and schizophrenia. It emerged that the severity of manic symptoms correlated with COMT activity in the striatum. The authors conclude that COMT striatal activity may serve as a biomarker for manic symptoms. Further studies are needed in order to confirm these results and to assess the neurobiological links between COMT activity and manic symptoms.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor