Pub Date : 2018-11-17DOI: 10.1080/15622975.2017.1282174
P. Geoffroy, E. Curis, C. Courtin, J. Moreira, Thomas Morvillers, B. Étain, J. Laplanche, F. Bellivier, C. Marie-Claire
Abstract Objectives: We examine whether the lithium response is associated with changes in the expression of core clock genes. Methods: The effect of a therapeutic concentration of lithium (1 mM) on the expression levels of 17 circadian genes was examined in lymphoblastoid cell lines (LCLs) derived from two well-characterized groups of bipolar disorder patients, defined as lithium non-responders (NR, n = 20) or excellent responders (ER, n = 16). Quantitative real-time PCR (qRT-PCR) was conducted at 2, 4 and 8 days (d2, d4 and d8) with and without lithium exposure. Results: At d2, in ER only, BHLHE41, RORA, PER1, ARNTL, CRY2, BHLHE40 and CSNK1D were upregulated, whereas NR1D1 was downregulated. At d4, in ER only, CRY1 was downregulated. At d8, in NR only, GSK3β was upregulated and DBP, TIMELESS and CRY1 were downregulated. Significant Group × Lithium interactions existed for NR1D1 at d2 (P = 0.02), and CRY1 at d4 (P = 0.02). Longitudinal analyses showed differential temporal evolutions between NR and ER (significant Time × Group interaction) for PER3, NR1D1, DBP, RORA, CSNK1D and TIMELESS; and a significant Time × Lithium interaction for NR1D1. Coexpression data analyses suggested distinct groups of circadian genes concurrently modulated by lithium. Conclusions: In LCLs, lithium influences expression of circadian genes with differences in amplitude and kinetics according to the patient’s lithium response status.
目的:我们研究锂反应是否与核心时钟基因的表达变化有关。方法:研究了锂治疗浓度(1mm)对来自两组特征明确的双相情感障碍患者的淋巴母细胞样细胞系(LCLs)中17个昼夜节律基因表达水平的影响，这两组患者被定义为锂无反应(NR, n = 20)或良好反应(ER, n = 16)。在有和没有锂暴露的情况下，分别在第2、4和8天(d2、d4和d8)进行实时荧光定量PCR (qRT-PCR)检测。结果:d2时，仅ER组BHLHE41、RORA、PER1、ARNTL、CRY2、BHLHE40和CSNK1D上调，NR1D1下调。在第4天，仅在ER中，CRY1下调。d8时，仅在NR中，GSK3β上调，DBP、TIMELESS和CRY1下调。NR1D1在d2时(P = 0.02)， CRY1在d4时(P = 0.02)存在显著的组与锂相互作用。纵向分析显示，PER3、NR1D1、DBP、RORA、CSNK1D和TIMELESS在时间上与ER存在差异(显著的时间×组交互作用);NR1D1具有显著的时间与锂相互作用。共表达数据分析表明，锂同时调节了不同的昼夜节律基因群。结论:在LCLs中，锂会影响昼夜节律基因的表达，并根据患者的锂反应状态在幅度和动力学上存在差异。
{"title":"Lithium response in bipolar disorders and core clock genes expression","authors":"P. Geoffroy, E. Curis, C. Courtin, J. Moreira, Thomas Morvillers, B. Étain, J. Laplanche, F. Bellivier, C. Marie-Claire","doi":"10.1080/15622975.2017.1282174","DOIUrl":"https://doi.org/10.1080/15622975.2017.1282174","url":null,"abstract":"Abstract Objectives: We examine whether the lithium response is associated with changes in the expression of core clock genes. Methods: The effect of a therapeutic concentration of lithium (1 mM) on the expression levels of 17 circadian genes was examined in lymphoblastoid cell lines (LCLs) derived from two well-characterized groups of bipolar disorder patients, defined as lithium non-responders (NR, n = 20) or excellent responders (ER, n = 16). Quantitative real-time PCR (qRT-PCR) was conducted at 2, 4 and 8 days (d2, d4 and d8) with and without lithium exposure. Results: At d2, in ER only, BHLHE41, RORA, PER1, ARNTL, CRY2, BHLHE40 and CSNK1D were upregulated, whereas NR1D1 was downregulated. At d4, in ER only, CRY1 was downregulated. At d8, in NR only, GSK3β was upregulated and DBP, TIMELESS and CRY1 were downregulated. Significant Group × Lithium interactions existed for NR1D1 at d2 (P = 0.02), and CRY1 at d4 (P = 0.02). Longitudinal analyses showed differential temporal evolutions between NR and ER (significant Time × Group interaction) for PER3, NR1D1, DBP, RORA, CSNK1D and TIMELESS; and a significant Time × Lithium interaction for NR1D1. Coexpression data analyses suggested distinct groups of circadian genes concurrently modulated by lithium. Conclusions: In LCLs, lithium influences expression of circadian genes with differences in amplitude and kinetics according to the patient’s lithium response status.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"7 1","pages":"619 - 632"},"PeriodicalIF":0.0,"publicationDate":"2018-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89961527","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 : 2018-11-17DOI: 10.1080/15622975.2017.1282172
E. Milanesi, R. Zanardini, G. Rosso, G. Maina, A. Barbon, C. Mora, A. Minelli, M. Gennarelli, L. Bocchio-Chiavetto
Abstract Objectives: Insulin-like growth factor binding protein 2 (IGFBP2) is a member of the family of high-affinity binding proteins (IGFBP1–6) and appears to play a governing role in insulin-like growth factor (IGF) regulation in the central nervous system. This study aimed to investigate the putative involvement of IGFBP2 in mood disorder pathogenesis by measuring its expression levels in patient peripheral tissues. Methods: IGFBP2 protein and mRNA levels were measured in the serum of 93 controls, 41 bipolar disorder (BD) and 43 major depressive disorder (MDD) patients and in the skin fibroblasts from 15 controls, 12 BD and 23 MDD patients. Results: The results indicated reduced expression of IGFBP2 in both tissues of BD patients, whereas no difference was found in MDD patients compared with controls. Conclusions: Our findings in peripheral tissues are consistent with previous results in the brain and support a downregulation of IGFBP2 expression that is specific for BD, suggesting a role for this protein in the alterations in neurodevelopment and neuroprotection observed in the disorder. Further studies in independent and larger cohorts are warranted to confirm the involvement of IGFBP2 in BD.
{"title":"Insulin-like growth factor binding protein 2 in bipolar disorder: An expression study in peripheral tissues","authors":"E. Milanesi, R. Zanardini, G. Rosso, G. Maina, A. Barbon, C. Mora, A. Minelli, M. Gennarelli, L. Bocchio-Chiavetto","doi":"10.1080/15622975.2017.1282172","DOIUrl":"https://doi.org/10.1080/15622975.2017.1282172","url":null,"abstract":"Abstract Objectives: Insulin-like growth factor binding protein 2 (IGFBP2) is a member of the family of high-affinity binding proteins (IGFBP1–6) and appears to play a governing role in insulin-like growth factor (IGF) regulation in the central nervous system. This study aimed to investigate the putative involvement of IGFBP2 in mood disorder pathogenesis by measuring its expression levels in patient peripheral tissues. Methods: IGFBP2 protein and mRNA levels were measured in the serum of 93 controls, 41 bipolar disorder (BD) and 43 major depressive disorder (MDD) patients and in the skin fibroblasts from 15 controls, 12 BD and 23 MDD patients. Results: The results indicated reduced expression of IGFBP2 in both tissues of BD patients, whereas no difference was found in MDD patients compared with controls. Conclusions: Our findings in peripheral tissues are consistent with previous results in the brain and support a downregulation of IGFBP2 expression that is specific for BD, suggesting a role for this protein in the alterations in neurodevelopment and neuroprotection observed in the disorder. Further studies in independent and larger cohorts are warranted to confirm the involvement of IGFBP2 in BD.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"19 1","pages":"610 - 618"},"PeriodicalIF":0.0,"publicationDate":"2018-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72658201","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 : 2018-11-15DOI: 10.1080/15622975.2016.1274051
Jian Li, Yanqing Tang, F. Womer, G. Fan, Qian Zhou, Wenge Sun, Ke Xu, Fei Wang
Abstract Objectives: Bipolar disorder (BD) and schizophrenia (SZ) share structural abnormalities in the anterior insula cortex (AIC). The AIC appears to have a crucial role in emotional processing and regulation and cognitive control in BD and SZ. Methods: Forty-six participants with BD, 68 with SZ and 66 healthy controls (HC) underwent functional magnetic resonance imaging scanning. Resting-state functional connectivity (rsFC) from AIC subregions (ventral and dorsal) was compared among the three groups. Results: Compared to HC group, both BD and SZ groups exhibited increased rsFC from the ventral AIC (vAIC) and dorsal AIC (dAIC) to bilateral frontal pole and thalamus, the left middle frontal gyrus and the hippocampus. Meanwhile, the BD group demonstrated increased rsFC from the vAIC to the perigenual anterior cingulate cortex, the SZ group presented increased rsFC from the vAIC and dAIC to the right caudate. Compared with the BD group, the SZ group showed significantly increased rsFC from the vAIC and dAIC to the left middle frontal gyrus. Conclusions: The shared AIC rsFC abnormalities in both BD and SZ support the importance of the AIC in the common pathophysiology of BD and SZ. There were also disorder-specific features of AIC rsFC, which might implicate potential avenues for differentiating during the early stages.
{"title":"Two patterns of anterior insular cortex functional connectivity in bipolar disorder and schizophrenia","authors":"Jian Li, Yanqing Tang, F. Womer, G. Fan, Qian Zhou, Wenge Sun, Ke Xu, Fei Wang","doi":"10.1080/15622975.2016.1274051","DOIUrl":"https://doi.org/10.1080/15622975.2016.1274051","url":null,"abstract":"Abstract Objectives: Bipolar disorder (BD) and schizophrenia (SZ) share structural abnormalities in the anterior insula cortex (AIC). The AIC appears to have a crucial role in emotional processing and regulation and cognitive control in BD and SZ. Methods: Forty-six participants with BD, 68 with SZ and 66 healthy controls (HC) underwent functional magnetic resonance imaging scanning. Resting-state functional connectivity (rsFC) from AIC subregions (ventral and dorsal) was compared among the three groups. Results: Compared to HC group, both BD and SZ groups exhibited increased rsFC from the ventral AIC (vAIC) and dorsal AIC (dAIC) to bilateral frontal pole and thalamus, the left middle frontal gyrus and the hippocampus. Meanwhile, the BD group demonstrated increased rsFC from the vAIC to the perigenual anterior cingulate cortex, the SZ group presented increased rsFC from the vAIC and dAIC to the right caudate. Compared with the BD group, the SZ group showed significantly increased rsFC from the vAIC and dAIC to the left middle frontal gyrus. Conclusions: The shared AIC rsFC abnormalities in both BD and SZ support the importance of the AIC in the common pathophysiology of BD and SZ. There were also disorder-specific features of AIC rsFC, which might implicate potential avenues for differentiating during the early stages.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"1 1","pages":"S115 - S123"},"PeriodicalIF":0.0,"publicationDate":"2018-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89836710","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 : 2018-11-15DOI: 10.1080/15622975.2016.1262061
A. Tiwari, Danning Zhang, Jennie G Pouget, C. Zai, N. Chowdhury, E. Brandl, L. Qin, Natalie Freeman, J. Lieberman, H. Meltzer, J. Kennedy, D. Müller
Abstract Objectives: A positive correlation between antipsychotic-induced weight gain (AIWG) and the antagonist effect of antipsychotic drugs at the histamine H1 receptor (HRH1) as well as the agonist effect at the histamine H3 receptor (HRH3) in the brain has been consistently demonstrated. We investigated the potential impact of single-nucleotide polymorphisms (SNPs) in HRH1 and HRH3 genes on AIWG. Methods: We analysed 40 tagSNPs in HRH1 (n = 34) and HRH3 (n = 6) in schizophrenia/schizoaffective disorder patients (n = 193) primarily treated with clozapine or olanzapine for up to 14 weeks. Linear regression was used to evaluate the association between SNPs and AIWG, with baseline weight and treatment duration as covariates. Results: In HRH1, a nominal association of rs7639145 with AIWG was observed in patients of European ancestry treated with either clozapine or olanzapine (P = 0.043; β = 1.658; n = 77). We observed nominal association for two HRH1 SNPs rs346074 (P = 0.002; β = –5.024) and rs13064530 (P = 0.004; β = –5.158) in patients of African ancestry treated with either clozapine or olanzapine (n = 37). However, the above associations are not significant after correcting for multiple testing. In HRH3, we did not observe association in either ancestry. Conclusions: The current study suggests that SNPs in HRH1 and HRH3 may not have a major role in AIWG.
{"title":"Impact of histamine receptors H1 and H3 polymorphisms on antipsychotic-induced weight gain","authors":"A. Tiwari, Danning Zhang, Jennie G Pouget, C. Zai, N. Chowdhury, E. Brandl, L. Qin, Natalie Freeman, J. Lieberman, H. Meltzer, J. Kennedy, D. Müller","doi":"10.1080/15622975.2016.1262061","DOIUrl":"https://doi.org/10.1080/15622975.2016.1262061","url":null,"abstract":"Abstract Objectives: A positive correlation between antipsychotic-induced weight gain (AIWG) and the antagonist effect of antipsychotic drugs at the histamine H1 receptor (HRH1) as well as the agonist effect at the histamine H3 receptor (HRH3) in the brain has been consistently demonstrated. We investigated the potential impact of single-nucleotide polymorphisms (SNPs) in HRH1 and HRH3 genes on AIWG. Methods: We analysed 40 tagSNPs in HRH1 (n = 34) and HRH3 (n = 6) in schizophrenia/schizoaffective disorder patients (n = 193) primarily treated with clozapine or olanzapine for up to 14 weeks. Linear regression was used to evaluate the association between SNPs and AIWG, with baseline weight and treatment duration as covariates. Results: In HRH1, a nominal association of rs7639145 with AIWG was observed in patients of European ancestry treated with either clozapine or olanzapine (P = 0.043; β = 1.658; n = 77). We observed nominal association for two HRH1 SNPs rs346074 (P = 0.002; β = –5.024) and rs13064530 (P = 0.004; β = –5.158) in patients of African ancestry treated with either clozapine or olanzapine (n = 37). However, the above associations are not significant after correcting for multiple testing. In HRH3, we did not observe association in either ancestry. Conclusions: The current study suggests that SNPs in HRH1 and HRH3 may not have a major role in AIWG.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"68 1","pages":"S105 - S97"},"PeriodicalIF":0.0,"publicationDate":"2018-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77152965","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 : 2018-10-31DOI: 10.1080/15622975.2016.1273549
Jasmine B. Taylor, Tarrant D. R. Cummins, A. Fox, B. Johnson, J. Tong, T. Visser, Z. Hawi, M. Bellgrove
Abstract Objectives: Previous studies have postulated that noradrenergic and/or dopaminergic gene variations are likely to underlie individual differences in impulsiveness, however, few have shown this. The current study examined the relationship between catecholamine gene variants and self-reported impulsivity, as measured by the Barratt Impulsiveness Scale (Version 11; BIS-11) Methods: Six hundred and seventy-seven non-clinical adults completed the Barratt Impulsiveness Scale (BIS-11). DNA was analysed for a set of 142 single-nucleotide polymorphisms (SNPs) across 20 autosomal catecholamine genes. Association was tested using an additive regression model with permutation testing used to control for the influence of multiple comparison. Results: Analysis revealed an influence of rs4245146 of the dopamine D2 receptor (DRD2) gene on the BIS-11 attention first-order factor, such that self-reported attentional impulsiveness increased in an additive fashion with each copy of the T allele. Conclusions: These findings provide preliminary evidence that allelic variation in DRD2 may influence impulsiveness by increasing the propensity for attentional lapses.
{"title":"Allelic variation in dopamine D2 receptor gene is associated with attentional impulsiveness on the Barratt Impulsiveness Scale (BIS-11)","authors":"Jasmine B. Taylor, Tarrant D. R. Cummins, A. Fox, B. Johnson, J. Tong, T. Visser, Z. Hawi, M. Bellgrove","doi":"10.1080/15622975.2016.1273549","DOIUrl":"https://doi.org/10.1080/15622975.2016.1273549","url":null,"abstract":"Abstract Objectives: Previous studies have postulated that noradrenergic and/or dopaminergic gene variations are likely to underlie individual differences in impulsiveness, however, few have shown this. The current study examined the relationship between catecholamine gene variants and self-reported impulsivity, as measured by the Barratt Impulsiveness Scale (Version 11; BIS-11) Methods: Six hundred and seventy-seven non-clinical adults completed the Barratt Impulsiveness Scale (BIS-11). DNA was analysed for a set of 142 single-nucleotide polymorphisms (SNPs) across 20 autosomal catecholamine genes. Association was tested using an additive regression model with permutation testing used to control for the influence of multiple comparison. Results: Analysis revealed an influence of rs4245146 of the dopamine D2 receptor (DRD2) gene on the BIS-11 attention first-order factor, such that self-reported attentional impulsiveness increased in an additive fashion with each copy of the T allele. Conclusions: These findings provide preliminary evidence that allelic variation in DRD2 may influence impulsiveness by increasing the propensity for attentional lapses.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"41 1","pages":"S75 - S83"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87206890","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 : 2018-10-31DOI: 10.1080/15622975.2016.1249950
Kamyar Keramatian, T. Dhanoa, A. McGirr, D. Lang, W. Honer, R. Lam, L. Yatham
Abstract Objectives: The neurobiological underpinnings of bipolar I disorder are not yet understood. Previous structural neuroimaging studies of bipolar disorder have produced rather conflicting results. We hypothesise that clinical sub-phenotypes of bipolar I disorder defined by their psychotic symptoms, especially those with mood-incongruent psychotic features, may have more extensive structural brain abnormalities. Methods: We investigated structural brain alterations in patients with first-episode mania (n = 55) with mood-congruent (n = 16) and mood-incongruent (n = 32) psychotic features, as well as those without psychotic symptoms (n = 7), relative to healthy subjects (n = 56). Results: Total intracranial volume was significantly reduced in patients with mood-incongruent psychosis compared to healthy subjects while cerebrospinal fluid (CSF) volume was significantly increased. Patients with mood-congruent psychosis showed significant reduction in total white matter volume and significant CSF volume increase. Patients with psychosis had significant volume reduction in anterior cingulate and medial prefrontal cortices. Relative to mood-congruent psychotic features, mood-incongruent psychotic features were associated with volume reduction in the left middle temporal gyrus, right inferior parietal gyrus, right fusiform gyrus, left middle orbitofrontal gyrus and cerebellum. Conclusions: While preliminary, our findings suggest that the presence and type of psychosis in first-episode mania may be phenotypic markers of underlying biological variants of bipolar disorder.
{"title":"Structural brain changes in first episode mania with and without psychosis: Data from the Systematic Treatment Optimization Program for Early Mania (STOP-EM)","authors":"Kamyar Keramatian, T. Dhanoa, A. McGirr, D. Lang, W. Honer, R. Lam, L. Yatham","doi":"10.1080/15622975.2016.1249950","DOIUrl":"https://doi.org/10.1080/15622975.2016.1249950","url":null,"abstract":"Abstract Objectives: The neurobiological underpinnings of bipolar I disorder are not yet understood. Previous structural neuroimaging studies of bipolar disorder have produced rather conflicting results. We hypothesise that clinical sub-phenotypes of bipolar I disorder defined by their psychotic symptoms, especially those with mood-incongruent psychotic features, may have more extensive structural brain abnormalities. Methods: We investigated structural brain alterations in patients with first-episode mania (n = 55) with mood-congruent (n = 16) and mood-incongruent (n = 32) psychotic features, as well as those without psychotic symptoms (n = 7), relative to healthy subjects (n = 56). Results: Total intracranial volume was significantly reduced in patients with mood-incongruent psychosis compared to healthy subjects while cerebrospinal fluid (CSF) volume was significantly increased. Patients with mood-congruent psychosis showed significant reduction in total white matter volume and significant CSF volume increase. Patients with psychosis had significant volume reduction in anterior cingulate and medial prefrontal cortices. Relative to mood-congruent psychotic features, mood-incongruent psychotic features were associated with volume reduction in the left middle temporal gyrus, right inferior parietal gyrus, right fusiform gyrus, left middle orbitofrontal gyrus and cerebellum. Conclusions: While preliminary, our findings suggest that the presence and type of psychosis in first-episode mania may be phenotypic markers of underlying biological variants of bipolar disorder.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"27 1","pages":"S30 - S40"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77979648","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 : 2018-10-31DOI: 10.1080/15622975.2016.1258491
L. Kornmayer, G. Leicht, C. Mulert
Abstract Objectives: Aberrant salience mainly is attributed to excessive dopaminergic processing in the ventral striatum. Increased gamma power during sensory processing of physical salience has been shown to be associated with positive trait schizotypy. In the present study, this is assessed in patients with schizophrenia. Methods: The early evoked visual gamma-band response (GBR) at 40 Hz was assessed for a schizophrenia patient group (N = 22) and a matched healthy control group (N = 22) applying EEG time-frequency analysis. The GBR was assessed for two conditions within a visual detection paradigm: a target with or without a physically salient distracter and evaluated in relation to the PANSS. Results: A 2 × 2 ANOVA revealed a significant main effect of condition and a trend interaction of group and condition for the GBR, with highest power for schizophrenia patients in the physically salient distracter condition. Moreover, evoked GBR power in this condition was correlated with positive (r = 0.664; P = 0.001**) and disorganised (r = 0.618; P = 0.002**) schizophrenia symptoms. Conclusions: Evoked GBR power during processing of physical salience in schizophrenia was associated with positive symptoms. We suggest that abnormal processing of physically salient stimuli might be involved in the pathophysiological genesis of positive symptoms.
{"title":"Attentional capture by physically salient stimuli in the gamma frequency is associated with schizophrenia symptoms","authors":"L. Kornmayer, G. Leicht, C. Mulert","doi":"10.1080/15622975.2016.1258491","DOIUrl":"https://doi.org/10.1080/15622975.2016.1258491","url":null,"abstract":"Abstract Objectives: Aberrant salience mainly is attributed to excessive dopaminergic processing in the ventral striatum. Increased gamma power during sensory processing of physical salience has been shown to be associated with positive trait schizotypy. In the present study, this is assessed in patients with schizophrenia. Methods: The early evoked visual gamma-band response (GBR) at 40 Hz was assessed for a schizophrenia patient group (N = 22) and a matched healthy control group (N = 22) applying EEG time-frequency analysis. The GBR was assessed for two conditions within a visual detection paradigm: a target with or without a physically salient distracter and evaluated in relation to the PANSS. Results: A 2 × 2 ANOVA revealed a significant main effect of condition and a trend interaction of group and condition for the GBR, with highest power for schizophrenia patients in the physically salient distracter condition. Moreover, evoked GBR power in this condition was correlated with positive (r = 0.664; P = 0.001**) and disorganised (r = 0.618; P = 0.002**) schizophrenia symptoms. Conclusions: Evoked GBR power during processing of physical salience in schizophrenia was associated with positive symptoms. We suggest that abnormal processing of physically salient stimuli might be involved in the pathophysiological genesis of positive symptoms.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"12 1","pages":"S52 - S62"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72690155","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 : 2018-10-31DOI: 10.1080/15622975.2016.1252465
D. Cox, M. Gottschalk, V. Stelzhammer, Hendrik Wesseling, J. Cooper, S. Bahn
Abstract Objectives: Rodent models of major depressive disorder (MDD) are indispensable when screening for novel treatments, but assessing their translational relevance with human brain pathology has proved difficult. Methods: Using a novel systems approach, proteomics data obtained from post-mortem MDD anterior prefrontal cortex tissue (n = 12) and matched controls (n = 23) were compared with equivalent data from three commonly used preclinical models exposed to environmental stressors (chronic mild stress, prenatal stress and social defeat). Functional pathophysiological features associated with depression-like behaviour were identified in these models through enrichment of protein–protein interaction networks. A cross-species comparison evaluated which model(s) represent human MDD pathology most closely. Results: Seven functional domains associated with MDD and represented across at least two models such as “carbohydrate metabolism and cellular respiration” were identified. Through statistical evaluation using kernel-based machine learning techniques, the social defeat model was found to represent MDD brain changes most closely for four of the seven domains. Conclusions: This is the first study to apply a method for directly evaluating the relevance of the molecular pathology of multiple animal models to human MDD on the functional level. The methodology and findings outlined here could help to overcome translational obstacles of preclinical psychiatric research.
{"title":"Evaluation of molecular brain changes associated with environmental stress in rodent models compared to human major depressive disorder: A proteomic systems approach","authors":"D. Cox, M. Gottschalk, V. Stelzhammer, Hendrik Wesseling, J. Cooper, S. Bahn","doi":"10.1080/15622975.2016.1252465","DOIUrl":"https://doi.org/10.1080/15622975.2016.1252465","url":null,"abstract":"Abstract Objectives: Rodent models of major depressive disorder (MDD) are indispensable when screening for novel treatments, but assessing their translational relevance with human brain pathology has proved difficult. Methods: Using a novel systems approach, proteomics data obtained from post-mortem MDD anterior prefrontal cortex tissue (n = 12) and matched controls (n = 23) were compared with equivalent data from three commonly used preclinical models exposed to environmental stressors (chronic mild stress, prenatal stress and social defeat). Functional pathophysiological features associated with depression-like behaviour were identified in these models through enrichment of protein–protein interaction networks. A cross-species comparison evaluated which model(s) represent human MDD pathology most closely. Results: Seven functional domains associated with MDD and represented across at least two models such as “carbohydrate metabolism and cellular respiration” were identified. Through statistical evaluation using kernel-based machine learning techniques, the social defeat model was found to represent MDD brain changes most closely for four of the seven domains. Conclusions: This is the first study to apply a method for directly evaluating the relevance of the molecular pathology of multiple animal models to human MDD on the functional level. The methodology and findings outlined here could help to overcome translational obstacles of preclinical psychiatric research.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"78 1","pages":"S63 - S74"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82297908","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 : 2018-10-31DOI: 10.1080/15622975.2016.1273550
N. Monroy-Jaramillo, Elena Dyukova, C. Walss-Bass
Abstract Objectives: Psychiatric and substance-use disorders have been associated with premature biological ageing. Telomere length (TL), considered an ageing marker, has been analysed in psychiatric disorders, and to a lesser extent in substance-use disorders, with recent findings suggesting TL may be related to disease pathology. Methods: We conducted a critical and non-systematic literature search of TL studies published up to June 2016 in psychiatric and substance-use disorders, focussing on studies describing mechanisms, including studies linking telomere biology with genetic factors, stress and mitochondrial alterations (104 studies selected). Results: Patients with major depressive disorder and anxiety appear to have shorter leukocyte telomeres compared to controls. Inconclusive results are found for other psychiatric disorders and for substance-use disorders. This may be due in part to differences in medication treatment and response, as studies suggest that some psychotropic medications may modulate TL. Importantly, some studies establish a relationship between telomere machinery, stress and mitochondria function in psychiatric and substance-use disorders. Conclusions: While further longitudinal studies considering telomere genetics are needed to clarify the cause–effect link between telomeres and mitochondria function in psychiatric and substance-use disorders, the recent findings linking these biological processes suggest that telomeres may be more than ageing markers.
{"title":"Telomere length in psychiatric disorders: Is it more than an ageing marker?","authors":"N. Monroy-Jaramillo, Elena Dyukova, C. Walss-Bass","doi":"10.1080/15622975.2016.1273550","DOIUrl":"https://doi.org/10.1080/15622975.2016.1273550","url":null,"abstract":"Abstract Objectives: Psychiatric and substance-use disorders have been associated with premature biological ageing. Telomere length (TL), considered an ageing marker, has been analysed in psychiatric disorders, and to a lesser extent in substance-use disorders, with recent findings suggesting TL may be related to disease pathology. Methods: We conducted a critical and non-systematic literature search of TL studies published up to June 2016 in psychiatric and substance-use disorders, focussing on studies describing mechanisms, including studies linking telomere biology with genetic factors, stress and mitochondrial alterations (104 studies selected). Results: Patients with major depressive disorder and anxiety appear to have shorter leukocyte telomeres compared to controls. Inconclusive results are found for other psychiatric disorders and for substance-use disorders. This may be due in part to differences in medication treatment and response, as studies suggest that some psychotropic medications may modulate TL. Importantly, some studies establish a relationship between telomere machinery, stress and mitochondria function in psychiatric and substance-use disorders. Conclusions: While further longitudinal studies considering telomere genetics are needed to clarify the cause–effect link between telomeres and mitochondria function in psychiatric and substance-use disorders, the recent findings linking these biological processes suggest that telomeres may be more than ageing markers.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"1 1","pages":"S2 - S20"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86671632","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 : 2018-10-31DOI: 10.1080/15622975.2016.1259498
M. Pantović-Stefanović, N. Petronijević, B. Dunjić-Kostić, M. Velimirović, T. Nikolić, V. Jurišić, M. Lačković, A. Damjanović, S. Totić-Poznanović, A. Jovanović, M. Ivković
Abstract Objectives: To explore the serum levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular cell adhesion molecule-1 (sICAM-1), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in patients with bipolar disorder (BD), with regard to acute episode characteristics, course of the disorder and treatment. Methods: The study group consisted of 83 patients diagnosed with BD type I. The control group consisted of 73 healthy individuals, matched with the study group according to age, gender and body mass index. The serum levels of sVCAM-1, sICAM-1, TNF-α and IL-6 were measured by ELISA. Results: Compared with healthy controls, significantly elevated levels of IL-6 and sICAM-1 and significantly lower levels of TNF-α and sVCAM-1 were identified in acute and remission phases of BD. The acute serum levels of sVCAM-1 were associated with the type and severity of acute mood symptoms as well as with course of illness characteristics. TNF-α was associated with duration of untreated disorder and type of treatment. Conclusions: BD is related to both acute and long-term alterations of immune mediators, including adhesion molecules. The potential immunomodulatory role of pharmacotherapeutic treatment is also to be considered in BD.
{"title":"sVCAM-1, sICAM-1, TNF-α and IL-6 levels in bipolar disorder type I: Acute, longitudinal and therapeutic implications","authors":"M. Pantović-Stefanović, N. Petronijević, B. Dunjić-Kostić, M. Velimirović, T. Nikolić, V. Jurišić, M. Lačković, A. Damjanović, S. Totić-Poznanović, A. Jovanović, M. Ivković","doi":"10.1080/15622975.2016.1259498","DOIUrl":"https://doi.org/10.1080/15622975.2016.1259498","url":null,"abstract":"Abstract Objectives: To explore the serum levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular cell adhesion molecule-1 (sICAM-1), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in patients with bipolar disorder (BD), with regard to acute episode characteristics, course of the disorder and treatment. Methods: The study group consisted of 83 patients diagnosed with BD type I. The control group consisted of 73 healthy individuals, matched with the study group according to age, gender and body mass index. The serum levels of sVCAM-1, sICAM-1, TNF-α and IL-6 were measured by ELISA. Results: Compared with healthy controls, significantly elevated levels of IL-6 and sICAM-1 and significantly lower levels of TNF-α and sVCAM-1 were identified in acute and remission phases of BD. The acute serum levels of sVCAM-1 were associated with the type and severity of acute mood symptoms as well as with course of illness characteristics. TNF-α was associated with duration of untreated disorder and type of treatment. Conclusions: BD is related to both acute and long-term alterations of immune mediators, including adhesion molecules. The potential immunomodulatory role of pharmacotherapeutic treatment is also to be considered in BD.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"435 1","pages":"S41 - S51"},"PeriodicalIF":0.0,"publicationDate":"2018-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83632779","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}
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