Dear colleagues,
It is my great pleasure to introduce to you the sixth issue of 2016 featuring the second part of the WFSBP Consensus Statement for biological markers and endophenotypes in schizophrenia as well as original research on biomarkers in schizophrenia.
The second part of WFSBP Consensus for biological markers and endophenotypes in schizophrenia reviews the current literature on biomarkers in schizophrenia, with the focus being on cognition, neuroimaging and genetics. The aim is to identify genetic underpinnings, clinical and cognitive endophenotypes and symptom dimensions of schizophrenia. Several identified biomarkers as possible candidates for future research are discussed. They propose that future studies should examine the effects of treatment and stage of the disease with the application of biomarker candidates.
Hýža and associates assessed the hippocampal volume in first-episode schizophrenia in a longitudinal prospective study. Baseline scans were analysed using voxel-based morphometry of the hippocampal fields. A significant negative correlation was detected between first-episode duration and baseline hippocampal morphology while later unfavourable course of schizophrenia had no correlation to baseline brain morphology, suggesting that there is no baseline morphological abnormality that predisposes to frequent psychotic outbursts.
In a schizophrenia mouse model, Shahriari et al., examined whether γ-band auditory steady-state electroencephalogram responses (ASSR) are reduced in power and phase locking. In mutant mice, they did detect reduced ASSR power. Furthermore, the phase locking was reduced in the γ–band in the auditory cortex. Their findings suggest that the model could be useful for preclinical studies of schizophrenia.
Yoshino and co-workers analysed methylation rates in the upstream region of dopamine receptor 2 (DRD2) in leukocytes of schizophrenic patients in comparison to controls. Seven CpG sites in the DRD2 region were analysed and indeed they found differences in methylation. The rates of methylation were significantly lower in medicated and drug naïve patients compared to controls. In conclusion, low methylation rates of DRD2 in leukocytes may be a trait biomarker for schizophrenia.
In a genetic meta-analysis, Chang and associates report on rs2312147 near the VRK2 gene in European and Asian populations, comparing schizophrenic patients with healthy controls. Genome-wide significance for the rs2312147 was detected for the European population while it did not reach significance in the Asian population. The results point to a certain susceptibility of the VRK2 gene to schizophrenia, specifically in European populations.
Yang and colleagues explored association between SCAP and SREBF1 gene polymorphisms and metabolic syndrome in schizophrenia patients treated with antipsychotics. What they found is that the T allele of rs11654081 of the SREBF1 gene was associated with increased risk of metabolic syndrome. They conclude that polymorphisms within the SREBF1 gene may play a role in the mechanism for inter-individual variation of antipsychotic induced metabolic syndrome.
In a brief report, Cuturic and associates compared serum carnitine levels and clinical correlates between stable outpatients and acutely hospitalized patients diagnosed with bipolar disorder or schizophrenia. Higher serum levels were detected in stable outpatients compared to acutely hospitalized patients. Additionally, metabolic syndrome was more common in outpatients. Results revealed a complicated relationship between carnitine levels, metabolic syndrome and behavioural outcomes.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor