Dear colleagues,
It is my great pleasure to introduce to you the second issue of 2019 featuring original research on Cannabidiol and Schizophrenia.
In a commentary, Gobbi discusses the published review on the role of cannabidiol (CBD) in psychiatry. The author outlines plausible factors that explain the scarcity of conclusions from preclinical and clinical studies on cannabidiol and highlights the appropriate measures and procedures to be employed in order for CBD to be considered and FDA-approved drug.
Machado Khoury and colleagues review the role of cannabidiol in psychiatry. Literature research revealed that most studies published presented several drawbacks and did not reach statistical significance. No evidence regarding major depressive and bipolar disorders have been found and only discrete adverse effects were reported.
Koethe et al., assessed familial abnormalities of endocannabinoid signalling in schizophrenia. The authors investigated the heritability of endocannabinoid signalling and found significantly higher levels of anandamide and palmitoylethanolimde in twins discordant for schizophrenia or bipolar disorder. The results suggest a protective upregulation of endocannabinoid signalling; reflecting either a hereditary trait or mirror a modulating response to genetically influenced cerebral function.
Piluso and associates assessed de novo copy-number variations (CNVs) in Italian patients with schizophrenia. In a sample of seven patients, de novo CNVs were found which encompass genes involved in brain development as well as one which is involved in a regulatory enhancer element responsible for the behavioural abnormalities in mutant mice. These findings provide further evidence for the involvement of de novo CNVs in the pathogenesis of schizophrenia and suggest that CNVs affecting regulatory enhancer elements could contribute to the genetic vulnerability to the disorder.
Jiménez-Trevino and colleagues aimed to investigate the effect of 5-HTTLPR-brain-derived neurotrophic factor (BDNF) gene interactions and early adverse life on impulsivity in suicide attempters. Interaction analysis showed that a combination of 5-HTTLPR-SS genotype and early trauma exposure increase impulsivity scores independently. However, impulsivity scores were not affected by the modulation of BDNF genes. The authors conclude that childhood trauma and 5-HTTLPR genotypes are independently involved in suicide attempts and share a common pathway of increasing impulsivity.
Xiao et al., assessed the elevated serum vascular endothelial growth factor (VEGF) in treatment-resistant schizophrenia (TRS) treated with electroconvulsive therapy (ECT). Pre-treatment serum VEGF levels were lower in TRS patients and increased significantly following ECT compared to controls. Also, a positive correlation between the change in VEGF and therapeutic effects was observed. The authors conclude that alterations in VEGF levels may constitute an index by which to evaluate the improvement in clinical condition.
In a brief report, García-Álvarez and colleagues examined the difference between early versus late stage schizophrenia. Early-stage schizophrenia showed greater negative symptom severity, lower levels of IκBα and were more frequently classified as normal weight compared to late-stage. Age and IκBα are the unique markers that differentiate between early- and late-stage schizophrenia patients. The results support the hypothesis of toxicity of episodes and highlight the importance of preventing new episodes.
Yours sincerely,
Siegfried Kasper, MD
Chief Editor