Pub Date : 2019-11-21DOI: 10.1080/15622975.2019.1696474
A. Pan, E. Ryu, J. Geske, Xinyang Zhou, S. McElroy, M. Cicek, M. Frye, J. Biernacka, A. Andreazza
Abstract Objectives: To investigate the effect of sample handling on inflammatory cytokines in serum and highlight challenges with using samples pre-collected from biobanks for biomarker research. Methods: Cytokine concentrations (IL-1β, IL-2, IL-6, IL-8, IL-10, TNFα, and IFNγ) were measured in serum samples of 205 patients with bipoldar disorder (BD) from the Mayo Clinic Bipolar Disorder Biobank and 205 non-psychiatric controls from the Mayo Clinic Biobank. As cytokine concentrations varied by recruitment site, post-hoc models were used to test the effect of clinical variables and pre-processing time on cytokines. To evaluate the effect of pre-processing time experimentally, cytokines were assayed in serum and plasma from 6 healthy volunteers processed at different time points. Results: Cytokine levels were significantly higher in the BD group. However, both cytokine levels and pre-processing times differed by recruitment site, and post-hoc analyses revealed that pre-processing time was significantly associated with several cytokines. An experiment using samples from healthy volunteers confirmed that concentrations for most cytokines increased with longer pre-processing times. Conclusions: Delays in processing influence cytokine concentrations in blood samples. Given the increasing use of biobanks in research, this study highlights the need to carefully evaluate sample collection and handling methods when designing biomarker studies.
{"title":"The impact of sample processing on inflammatory markers in serum: Lessons learned","authors":"A. Pan, E. Ryu, J. Geske, Xinyang Zhou, S. McElroy, M. Cicek, M. Frye, J. Biernacka, A. Andreazza","doi":"10.1080/15622975.2019.1696474","DOIUrl":"https://doi.org/10.1080/15622975.2019.1696474","url":null,"abstract":"Abstract Objectives: To investigate the effect of sample handling on inflammatory cytokines in serum and highlight challenges with using samples pre-collected from biobanks for biomarker research. Methods: Cytokine concentrations (IL-1β, IL-2, IL-6, IL-8, IL-10, TNFα, and IFNγ) were measured in serum samples of 205 patients with bipoldar disorder (BD) from the Mayo Clinic Bipolar Disorder Biobank and 205 non-psychiatric controls from the Mayo Clinic Biobank. As cytokine concentrations varied by recruitment site, post-hoc models were used to test the effect of clinical variables and pre-processing time on cytokines. To evaluate the effect of pre-processing time experimentally, cytokines were assayed in serum and plasma from 6 healthy volunteers processed at different time points. Results: Cytokine levels were significantly higher in the BD group. However, both cytokine levels and pre-processing times differed by recruitment site, and post-hoc analyses revealed that pre-processing time was significantly associated with several cytokines. An experiment using samples from healthy volunteers confirmed that concentrations for most cytokines increased with longer pre-processing times. Conclusions: Delays in processing influence cytokine concentrations in blood samples. Given the increasing use of biobanks in research, this study highlights the need to carefully evaluate sample collection and handling methods when designing biomarker studies.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"15 1","pages":"230 - 237"},"PeriodicalIF":0.0,"publicationDate":"2019-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79030485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-16DOI: 10.1080/15622975.2019.1669822
F. Christidi, E. Karavasilis, L. Michels, F. Riederer, G. Velonakis, E. Anagnostou, P. Ferentinos, S. Kollias, E. Efstathopoulos, N. Kelekis, E. Kararizou
Abstract Objectives We examined the neuroanatomical substrate of different pain catastrophising (PC) dimensions (i.e. rumination; magnification; helplessness) in patients with medication-overuse headache (MOH). Methods We included 18 MOH patients who were administered the Pain Catastrophizing Scale (PCS) and scanned in a 3T-MRI. We conducted whole-brain volumetric and resting-state functional connectivity (FC) analysis to examine the association between grey matter (GM) density and FC strength and PCS dimensions controlling for depression and anxiety. Results Higher total PCS score was associated with decreased GM density in precentral and inferior temporal gyrus, increased FC between middle temporal gyrus and cerebellum and reduced FC between precuneus and inferior temporal gyrus, as well as between frontal pole and temporal fusiform cortex. Regarding PCS dimensions, we mainly observed the involvement of (1) somatosensory cortex, supramarginal gyrus, basal ganglia, core default-mode network (DMN) in rumination; (2) somatosensory cortex, core DMN, dorsal medial prefrontal cortex (DMPFC)-DMN subsystem and cerebellum in magnification; and (3) temporal regions, DMN and basal ganglia in helplessness. Conclusions PC dimensions are associated with a specific structural and functional neuroanatomical pattern, which is different from the pattern observed when PC is considered as a single score. The involvement of basal ganglia and cerebellum needs further investigation.
{"title":"Dimensions of pain catastrophising and specific structural and functional alterations in patients with chronic pain: Evidence in medication-overuse headache","authors":"F. Christidi, E. Karavasilis, L. Michels, F. Riederer, G. Velonakis, E. Anagnostou, P. Ferentinos, S. Kollias, E. Efstathopoulos, N. Kelekis, E. Kararizou","doi":"10.1080/15622975.2019.1669822","DOIUrl":"https://doi.org/10.1080/15622975.2019.1669822","url":null,"abstract":"Abstract Objectives We examined the neuroanatomical substrate of different pain catastrophising (PC) dimensions (i.e. rumination; magnification; helplessness) in patients with medication-overuse headache (MOH). Methods We included 18 MOH patients who were administered the Pain Catastrophizing Scale (PCS) and scanned in a 3T-MRI. We conducted whole-brain volumetric and resting-state functional connectivity (FC) analysis to examine the association between grey matter (GM) density and FC strength and PCS dimensions controlling for depression and anxiety. Results Higher total PCS score was associated with decreased GM density in precentral and inferior temporal gyrus, increased FC between middle temporal gyrus and cerebellum and reduced FC between precuneus and inferior temporal gyrus, as well as between frontal pole and temporal fusiform cortex. Regarding PCS dimensions, we mainly observed the involvement of (1) somatosensory cortex, supramarginal gyrus, basal ganglia, core default-mode network (DMN) in rumination; (2) somatosensory cortex, core DMN, dorsal medial prefrontal cortex (DMPFC)-DMN subsystem and cerebellum in magnification; and (3) temporal regions, DMN and basal ganglia in helplessness. Conclusions PC dimensions are associated with a specific structural and functional neuroanatomical pattern, which is different from the pattern observed when PC is considered as a single score. The involvement of basal ganglia and cerebellum needs further investigation.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"1 1","pages":"726 - 738"},"PeriodicalIF":0.0,"publicationDate":"2019-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89381872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-16DOI: 10.1080/15622975.2019.1669823
Srisaiyini Kidnapillai, C. Bortolasci, B. Panizzutti, Briana Spolding, T. Connor, K. Bonifácio, A. Sanigorski, O. Dean, T. Crowley, S. Jamain, L. Gray, M. Leboyer, M. Berk, K. Walder
Abstract Objectives: To understand the therapeutic mechanisms of bipolar disorder (BD) drugs at molecular and cellular levels. Methods: Next generation sequencing was used to determine the transcriptional effects of a combination of four commonly prescribed BD drugs (lithium, valproate, lamotrigine and quetiapine) or vehicle (0.2% DMSO) in NT2-N (human neuronal) cells and rats. Differential expression of genes and pathway analysis were performed using edgeR in R and Gene Set Enrichment Analysis software respectively. Free cholesterol levels and neurite outgrowth were quantified in NT2-N cells following combination and individual BD drug treatments. Results: Pathway analysis showed up-regulation of many elements of the cholesterol biosynthesis pathway in NT2-N cells and oxidative phosphorylation in rat brains. Intracellular cholesterol transport genes were upregulated (NPC1, NPC2 and APOE), while the cholesterol efflux gene (ABCA1) was downregulated. BD drug combination tended to increase intracellular cholesterol levels and neurite outgrowth, but these effects were not seen for the drugs when used individually. Conclusions: These data suggest that BD drug combination is increasing cholesterol biosynthesis and the newly synthesised cholesterol is being utilised within the cells, possibly for synthesis of new membranes to facilitate neurite outgrowth. This mechanism possibly underpins clinical efficacy in individuals with BD treated with polypharmacy.
目的:从分子和细胞水平了解双相情感障碍(BD)药物的治疗机制。方法:采用下一代测序方法测定四种常用BD药物(锂、丙戊酸盐、拉莫三嗪和喹硫平)或载体(0.2% DMSO)联合使用对NT2-N(人神经元)细胞和大鼠的转录作用。分别使用edgeR in R和Gene Set Enrichment analysis软件进行基因差异表达和通路分析。在联合和单独治疗双相障碍药物后，对NT2-N细胞的游离胆固醇水平和神经突生长进行量化。结果:通路分析显示，大鼠脑内NT2-N细胞和氧化磷酸化中胆固醇生物合成途径的许多元件上调。细胞内胆固醇转运基因(NPC1、NPC2和APOE)上调，而胆固醇外排基因(ABCA1)下调。双酚d药物联合使用倾向于增加细胞内胆固醇水平和神经突生长，但单独使用时没有观察到这些影响。结论:这些数据表明，双酚d药物联合使用增加了胆固醇的生物合成，新合成的胆固醇正在细胞内被利用，可能用于合成新的膜，促进神经突的生长。这一机制可能是多种药物治疗双相障碍患者临床疗效的基础。
{"title":"Drugs used in the treatment of bipolar disorder and their effects on cholesterol biosynthesis – A possible therapeutic mechanism","authors":"Srisaiyini Kidnapillai, C. Bortolasci, B. Panizzutti, Briana Spolding, T. Connor, K. Bonifácio, A. Sanigorski, O. Dean, T. Crowley, S. Jamain, L. Gray, M. Leboyer, M. Berk, K. Walder","doi":"10.1080/15622975.2019.1669823","DOIUrl":"https://doi.org/10.1080/15622975.2019.1669823","url":null,"abstract":"Abstract Objectives: To understand the therapeutic mechanisms of bipolar disorder (BD) drugs at molecular and cellular levels. Methods: Next generation sequencing was used to determine the transcriptional effects of a combination of four commonly prescribed BD drugs (lithium, valproate, lamotrigine and quetiapine) or vehicle (0.2% DMSO) in NT2-N (human neuronal) cells and rats. Differential expression of genes and pathway analysis were performed using edgeR in R and Gene Set Enrichment Analysis software respectively. Free cholesterol levels and neurite outgrowth were quantified in NT2-N cells following combination and individual BD drug treatments. Results: Pathway analysis showed up-regulation of many elements of the cholesterol biosynthesis pathway in NT2-N cells and oxidative phosphorylation in rat brains. Intracellular cholesterol transport genes were upregulated (NPC1, NPC2 and APOE), while the cholesterol efflux gene (ABCA1) was downregulated. BD drug combination tended to increase intracellular cholesterol levels and neurite outgrowth, but these effects were not seen for the drugs when used individually. Conclusions: These data suggest that BD drug combination is increasing cholesterol biosynthesis and the newly synthesised cholesterol is being utilised within the cells, possibly for synthesis of new membranes to facilitate neurite outgrowth. This mechanism possibly underpins clinical efficacy in individuals with BD treated with polypharmacy.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"62 1","pages":"766 - 777"},"PeriodicalIF":0.0,"publicationDate":"2019-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86846413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-09DOI: 10.1080/15622975.2019.1663929
Qin-yu Lv, Yanhong Guo, Minghuan Zhu, Ruijie Geng, Xiaoyan Cheng, Chenxi Bao, Yingyi Wang, Xinxin Huang, Chen Zhang, Y. Hao, Zezhi Li, Z. Yi
Abstract Objectives: This is the first study to investigate the oxidative stress (OxS) levels in drug-free bipolar disorder (BD) patients and their association with lithium response. Methods: A total of 61 drug-free BD patients and 49 controls were included. Patients treated with lithium were followed-up for 6 weeks. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) were measured at baseline and at the end of the sixth week. Results: Compared to controls, the SOD levels were lower, whereas the MDA were higher in the BD-depression (BD-D) group (both P < 0.001). GSH-Px levels were higher in both the BD-D and the BD-mania (BD-M) group (both P < 0.001). Both GSH-Px and MDA levels in the BD (P = 0.009, P < 0.001) and the BD-D subgroup (P = 0.006, P = 0.001) decreased significantly after the 6-week treatment with lithium. Interestingly, both GSH-Px and MDA levels decreased in responders (P = 0.03, P = 0.002) but not in the non-responders of BD-D (both p > 0.05). Moreover, the reduction in the MDA levels were associated with lithium response (B = 1.47, Wald statistic = 5.94, P = 0.015, odds ratio = 4.35, 95% confidence interval 1.33-14.20). Conclusions: Our study demonstrates an imbalance of OxS in drug-free BD, especially BD-D. Lithium reduces the GSH-Px and MDA levels in BD patients. The reduction in MDA levels may predict individual responsiveness to lithium.
{"title":"Predicting individual responses to lithium with oxidative stress markers in drug-free bipolar disorder","authors":"Qin-yu Lv, Yanhong Guo, Minghuan Zhu, Ruijie Geng, Xiaoyan Cheng, Chenxi Bao, Yingyi Wang, Xinxin Huang, Chen Zhang, Y. Hao, Zezhi Li, Z. Yi","doi":"10.1080/15622975.2019.1663929","DOIUrl":"https://doi.org/10.1080/15622975.2019.1663929","url":null,"abstract":"Abstract Objectives: This is the first study to investigate the oxidative stress (OxS) levels in drug-free bipolar disorder (BD) patients and their association with lithium response. Methods: A total of 61 drug-free BD patients and 49 controls were included. Patients treated with lithium were followed-up for 6 weeks. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and malondialdehyde (MDA) were measured at baseline and at the end of the sixth week. Results: Compared to controls, the SOD levels were lower, whereas the MDA were higher in the BD-depression (BD-D) group (both P < 0.001). GSH-Px levels were higher in both the BD-D and the BD-mania (BD-M) group (both P < 0.001). Both GSH-Px and MDA levels in the BD (P = 0.009, P < 0.001) and the BD-D subgroup (P = 0.006, P = 0.001) decreased significantly after the 6-week treatment with lithium. Interestingly, both GSH-Px and MDA levels decreased in responders (P = 0.03, P = 0.002) but not in the non-responders of BD-D (both p > 0.05). Moreover, the reduction in the MDA levels were associated with lithium response (B = 1.47, Wald statistic = 5.94, P = 0.015, odds ratio = 4.35, 95% confidence interval 1.33-14.20). Conclusions: Our study demonstrates an imbalance of OxS in drug-free BD, especially BD-D. Lithium reduces the GSH-Px and MDA levels in BD patients. The reduction in MDA levels may predict individual responsiveness to lithium.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"11 1","pages":"778 - 789"},"PeriodicalIF":0.0,"publicationDate":"2019-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87772857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-04DOI: 10.1080/15622975.2019.1671610
D. Wittekind, J. Kratzsch, R. Mergl, C. Enzenbach, V. Witte, A. Villringer, M. Kluge
Abstract Objectives Ghrelin, an orexigenic peptide hormone, promotes drug reward and is suspected to play a role in nicotine dependence. However, there is little data on whether ghrelin levels are associated with active and/or former smoking. The relationship between ghrelin serum levels and smoking status in a population-based sample of individuals was studied. Methods Total ghrelin was determined after an overnight fast in 1519 subjects participating in a population-based cohort study (‘LIFE-Adult’). Tobacco consumption was assessed using both the questionnaire and interview. Generalised linear models with gamma distribution and log-link function were performed to analyse the association of total serum ghrelin with smoking status and the association between serum ghrelin and the amount of tobacco consumed in active smokers. Results Ghrelin levels were positively associated with active, but not former smoking (OR = 1.095; p = .002). This association was not moderated by sex (interaction of ‘active smoking’ and sex: p = .346). Ghrelin levels were not associated with the amount of tobacco consumed in active smokers. Conclusions This study provides evidence that total ghrelin serum levels are positively associated with active smoking. No association was found for former smokers. A unique feature of the study is the large sample size.
{"title":"Higher fasting ghrelin serum levels in active smokers than in former and never-smokers","authors":"D. Wittekind, J. Kratzsch, R. Mergl, C. Enzenbach, V. Witte, A. Villringer, M. Kluge","doi":"10.1080/15622975.2019.1671610","DOIUrl":"https://doi.org/10.1080/15622975.2019.1671610","url":null,"abstract":"Abstract Objectives Ghrelin, an orexigenic peptide hormone, promotes drug reward and is suspected to play a role in nicotine dependence. However, there is little data on whether ghrelin levels are associated with active and/or former smoking. The relationship between ghrelin serum levels and smoking status in a population-based sample of individuals was studied. Methods Total ghrelin was determined after an overnight fast in 1519 subjects participating in a population-based cohort study (‘LIFE-Adult’). Tobacco consumption was assessed using both the questionnaire and interview. Generalised linear models with gamma distribution and log-link function were performed to analyse the association of total serum ghrelin with smoking status and the association between serum ghrelin and the amount of tobacco consumed in active smokers. Results Ghrelin levels were positively associated with active, but not former smoking (OR = 1.095; p = .002). This association was not moderated by sex (interaction of ‘active smoking’ and sex: p = .346). Ghrelin levels were not associated with the amount of tobacco consumed in active smokers. Conclusions This study provides evidence that total ghrelin serum levels are positively associated with active smoking. No association was found for former smokers. A unique feature of the study is the large sample size.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"13 1","pages":"748 - 756"},"PeriodicalIF":0.0,"publicationDate":"2019-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73164021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-09-11DOI: 10.1080/15622975.2019.1656820
Jing Shi, X. Zou, Ke Jiang, Feng Wang
Abstract Objectives Clinically, there is no effective therapy for postoperative cognitive dysfunction (POCD). Inflammation after surgery is closely associated with POCD. Methods In this study, we explored the role of sirtuin 1 (SIRT1) in POCD. POCD in mice was induced by cardiac surgery. The mRNA and protein levels of related genes were determined by real-time polymerase chain reaction and western blot, respectively. Plasma concentrations of inflammatory factors were measured using an ELISA kit. Novel object and novel location recognition tests were carried out to measure recognition ability. The Morris water maze (MWM) test was performed to measure learning and memory ability. Results There was a clear decrease in SIRT1 expression after POCD. The SIRT1 activator SRT1720 promoted recognition, learning, and memory ability of mice with POCD. Moreover, SRT1720 treatment greatly inhibited plasma inflammatory cytokine levels and TLR4 and P65 protein expression in the hippocampus of POCD mice. The effect of SRT1720 on POCD was in a TLR4-dependent manner. Conclusions SIRT1 mediates the improvement of cardiac surgery-induced postoperative cognitive dysfunction via the TLR4/NF-κB pathway.
{"title":"SIRT1 mediates improvement of cardiac surgery-induced postoperative cognitive dysfunction via the TLR4/NF-κB pathway","authors":"Jing Shi, X. Zou, Ke Jiang, Feng Wang","doi":"10.1080/15622975.2019.1656820","DOIUrl":"https://doi.org/10.1080/15622975.2019.1656820","url":null,"abstract":"Abstract Objectives Clinically, there is no effective therapy for postoperative cognitive dysfunction (POCD). Inflammation after surgery is closely associated with POCD. Methods In this study, we explored the role of sirtuin 1 (SIRT1) in POCD. POCD in mice was induced by cardiac surgery. The mRNA and protein levels of related genes were determined by real-time polymerase chain reaction and western blot, respectively. Plasma concentrations of inflammatory factors were measured using an ELISA kit. Novel object and novel location recognition tests were carried out to measure recognition ability. The Morris water maze (MWM) test was performed to measure learning and memory ability. Results There was a clear decrease in SIRT1 expression after POCD. The SIRT1 activator SRT1720 promoted recognition, learning, and memory ability of mice with POCD. Moreover, SRT1720 treatment greatly inhibited plasma inflammatory cytokine levels and TLR4 and P65 protein expression in the hippocampus of POCD mice. The effect of SRT1720 on POCD was in a TLR4-dependent manner. Conclusions SIRT1 mediates the improvement of cardiac surgery-induced postoperative cognitive dysfunction via the TLR4/NF-κB pathway.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"8 1","pages":"757 - 765"},"PeriodicalIF":0.0,"publicationDate":"2019-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86987787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-03DOI: 10.1080/15622975.2019.1635270
L. Bartova, M. Dold, A. Kautzky, C. Fabbri, M. Spies, A. Serretti, D. Souery, J. Mendlewicz, J. Zohar, S. Montgomery, A. Schosser, S. Kasper
Abstract Objectives: The overview outlines two decades of research from the European Group for the Study of Resistant Depression (GSRD) that fundamentally impacted evidence-based algorithms for diagnostics and psychopharmacotherapy of treatment-resistant depression (TRD). Methods: The GSRD staging model characterising response, non-response and resistance to antidepressant (AD) treatment was applied to 2762 patients in eight European countries. Results: In case of non-response, dose escalation and switching between different AD classes did not show superiority over continuation of original AD treatment. Predictors for TRD were symptom severity, duration of the current major depressive episode (MDE), suicidality, psychotic and melancholic features, comorbid anxiety and personality disorders, add-on treatment, non-response to the first AD, adverse effects, high occupational level, recurrent disease course, previous hospitalisations, positive family history of MDD, early age of onset and novel associations of single nucleoid polymorphisms (SNPs) within the PPP3CC, ST8SIA2, CHL1, GAP43 and ITGB3 genes and gene pathways associated with neuroplasticity, intracellular signalling and chromatin silencing. A prediction model reaching accuracy of above 0.7 highlighted symptom severity, suicidality, comorbid anxiety and lifetime MDEs as the most informative predictors for TRD. Applying machine-learning algorithms, a signature of three SNPs of the BDNF, PPP3CC and HTR2A genes and lacking melancholia predicted treatment response. Conclusions: The GSRD findings offer a unique and balanced perspective on TRD representing foundation for further research elaborating on specific clinical and genetic hypotheses and treatment strategies within appropriate study-designs, especially interaction-based models and randomized controlled trials.
{"title":"Results of the European Group for the Study of Resistant Depression (GSRD) — basis for further research and clinical practice","authors":"L. Bartova, M. Dold, A. Kautzky, C. Fabbri, M. Spies, A. Serretti, D. Souery, J. Mendlewicz, J. Zohar, S. Montgomery, A. Schosser, S. Kasper","doi":"10.1080/15622975.2019.1635270","DOIUrl":"https://doi.org/10.1080/15622975.2019.1635270","url":null,"abstract":"Abstract Objectives: The overview outlines two decades of research from the European Group for the Study of Resistant Depression (GSRD) that fundamentally impacted evidence-based algorithms for diagnostics and psychopharmacotherapy of treatment-resistant depression (TRD). Methods: The GSRD staging model characterising response, non-response and resistance to antidepressant (AD) treatment was applied to 2762 patients in eight European countries. Results: In case of non-response, dose escalation and switching between different AD classes did not show superiority over continuation of original AD treatment. Predictors for TRD were symptom severity, duration of the current major depressive episode (MDE), suicidality, psychotic and melancholic features, comorbid anxiety and personality disorders, add-on treatment, non-response to the first AD, adverse effects, high occupational level, recurrent disease course, previous hospitalisations, positive family history of MDD, early age of onset and novel associations of single nucleoid polymorphisms (SNPs) within the PPP3CC, ST8SIA2, CHL1, GAP43 and ITGB3 genes and gene pathways associated with neuroplasticity, intracellular signalling and chromatin silencing. A prediction model reaching accuracy of above 0.7 highlighted symptom severity, suicidality, comorbid anxiety and lifetime MDEs as the most informative predictors for TRD. Applying machine-learning algorithms, a signature of three SNPs of the BDNF, PPP3CC and HTR2A genes and lacking melancholia predicted treatment response. Conclusions: The GSRD findings offer a unique and balanced perspective on TRD representing foundation for further research elaborating on specific clinical and genetic hypotheses and treatment strategies within appropriate study-designs, especially interaction-based models and randomized controlled trials.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"5 1","pages":"427 - 448"},"PeriodicalIF":0.0,"publicationDate":"2019-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90053274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-03DOI: 10.1080/15622975.2019.1655226
D. Rujescu
{"title":"Letter from the new Editor-in-Chief","authors":"D. Rujescu","doi":"10.1080/15622975.2019.1655226","DOIUrl":"https://doi.org/10.1080/15622975.2019.1655226","url":null,"abstract":"","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"11 1","pages":"426 - 426"},"PeriodicalIF":0.0,"publicationDate":"2019-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81911254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-02-07DOI: 10.1080/15622975.2019.1586366
{"title":"Reviewers of the year 2018","authors":"","doi":"10.1080/15622975.2019.1586366","DOIUrl":"https://doi.org/10.1080/15622975.2019.1586366","url":null,"abstract":"","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"7 1","pages":"166 - 168"},"PeriodicalIF":0.0,"publicationDate":"2019-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78575674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-02-01DOI: 10.1080/15622975.2017.1285049
J. M. Khoury, Maila de Castro Lourenço das Neves, M. A. Roque, Daniela Alves de Brito Queiroz, André Augusto Corrêa de Freitas, Â. de Fátima, F. Moreira, F. Garcia
Abstract Objectives: Understanding whether cannabidiol (CBD) is useful and safe for the treatment of psychiatric disorders is essential to empower psychiatrists and patients to take good clinical decisions. Our aim was to conduct a systematic review regarding the benefits and adverse events (AEs) of CBD in the treatment of schizophrenia, psychotic disorders, anxiety disorders, depression, bipolar disorder and substance-use disorders. Methods: We conducted a literature search in PubMed, Scielo, and Clinicaltrials.gov databases. Evidence was classified according to the WFSBP task forces standards. Results: Bibliographic research yielded 692 records. After analysis, we included six case reports and seven trials, comprising 201 subjects. Most the studies published presented several drawbacks and did not reach statistical significance. We have not found evidence regarding major depressive and bipolar disorders. The level of evidence for cannabis withdrawal is B; cannabis addiction is C2; treatment of positive symptoms in schizophrenia and anxiety in social anxiety disorder is C1. Discrete or no AEs were reported. The most frequently reported AEs are sedation and dizziness. Conclusions: The evidence regarding efficacy and safety of CBD in psychiatry is still scarce. Further larger well-designed randomised controlled trials are required to assess the effects of CBD in psychiatric disorders.
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