Pub Date : 2024-04-28DOI: 10.1080/15622975.2024.2346096
Sisi Zheng, Sitong Feng, Nan Song, Guangyao Chen, Yuan Jia, Guofu Zhang, Min Liu, Xue Li, Yanzhe Ning, Dan Wang, Hongxiao Jia
Objectives: Depersonalization-derealization disorder (DPD) is a dissociative disorder that impairs cognitive function and occupational performance. Emerging evidence indicate the levels of tumor ne...
{"title":"The role of the immune system in depersonalization disorder","authors":"Sisi Zheng, Sitong Feng, Nan Song, Guangyao Chen, Yuan Jia, Guofu Zhang, Min Liu, Xue Li, Yanzhe Ning, Dan Wang, Hongxiao Jia","doi":"10.1080/15622975.2024.2346096","DOIUrl":"https://doi.org/10.1080/15622975.2024.2346096","url":null,"abstract":"Objectives: Depersonalization-derealization disorder (DPD) is a dissociative disorder that impairs cognitive function and occupational performance. Emerging evidence indicate the levels of tumor ne...","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"38 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140811875","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 : 2024-04-17DOI: 10.1080/15622975.2024.2342849
A. Klymenko, V. Nagibin, A. Horlova, Y. Dobropolska, R. Bohovyk, D. Stroy, D. Isaev, V. Dosenko
Objectives. Molecular mechanisms of post-traumatic stress disorder (PTSD) development have been analyzed by evaluati-ng changes in the expression level of long non-coding RNA (lncRNA) as a potentia...
{"title":"Downregulation of lncRNAs Gomafu, NONMMUT033604.2, and NONMMUT064397.2 in the hippocampus of mice with model of post-traumatic stress disorder","authors":"A. Klymenko, V. Nagibin, A. Horlova, Y. Dobropolska, R. Bohovyk, D. Stroy, D. Isaev, V. Dosenko","doi":"10.1080/15622975.2024.2342849","DOIUrl":"https://doi.org/10.1080/15622975.2024.2342849","url":null,"abstract":"Objectives. Molecular mechanisms of post-traumatic stress disorder (PTSD) development have been analyzed by evaluati-ng changes in the expression level of long non-coding RNA (lncRNA) as a potentia...","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"127 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140613335","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 : 2020-10-20DOI: 10.1080/15622975.2019.1679391
Marie Woelfer, Meng Li, L. Colic, T. Liebe, Xin Di, B. Biswal, J. Murrough, V. Lessmann, T. Brigadski, M. Walter
Abstract Objectives Synaptic plasticity and brain-derived neurotrophic factor (BDNF) signalling are proposed to play key roles in antidepressant drug action. Ketamine, an N-methyl-D-aspartate receptor antagonist and putative antidepressant, may increase synaptic plasticity in prefrontal cortex through higher expression of BDNF. Furthermore, ketamine was shown to change resting-state functional connectivity (RSFC) of dorsomedial prefrontal cortex (dmPFC). Methods In a randomised, placebo-controlled study, we investigated acutely (100 min) and at 24 h following subanesthetic ketamine infusion which dmPFC seeded RSFC changes are most strongly associated with plasma BDNF level changes in 53 healthy participants (21 females, age: 24.4 ± 2.9 years) using 7 T-fMRI. Results We observed higher relative levels of BDNF 2 h and 24 h after ketamine compared to placebo. Whole-brain regression revealed that the change in BDNF after 24 h was associated with RSFC decreases from dmPFC to posterior cingulate cortex and ventromedial PFC at 24 h and exploratively also at the 100 min measurement point. Follow-up analyses revealed that RSFC reductions following ketamine were restricted to subjects showing increased BDNF levels at 24 h. Conclusions Our findings indicate BDNF level dynamics following ketamine are related to acute and 24 h RSFC changes. Particularly when BDNF increases are observed after ketamine infusion, a disconnection from dmPFC after 24 h is seen and may reflect synaptic plasticity effects.
摘要目的突触可塑性和脑源性神经营养因子(BDNF)信号在抗抑郁药物作用中起关键作用。氯胺酮是一种n -甲基- d -天冬氨酸受体拮抗剂和公认的抗抑郁药，它可能通过提高BDNF的表达来增加前额叶皮层的突触可塑性。此外，氯胺酮被证明可以改变背内侧前额叶皮层(dmPFC)静息状态功能连接(RSFC)。方法在一项随机、安慰剂对照研究中，我们通过7次T-fMRI研究了53名健康参与者(21名女性，年龄:24.4±2.9岁)在亚麻醉氯胺酮输注后急性(100分钟)和24小时dmPFC种子RSFC变化与血浆BDNF水平变化最密切相关的情况。结果与安慰剂相比，氯胺酮治疗后2小时和24小时BDNF的相对水平较高。全脑回归显示24 h后BDNF的变化与RSFC在24 h从dmPFC到后扣带皮层和腹内侧PFC的减少有关，并且在100 min测点也具有探索性。随访分析显示，氯胺酮后RSFC降低仅限于24小时BDNF水平升高的受试者。结论氯胺酮后BDNF水平动态变化与急性和24 h RSFC变化有关。特别是当氯胺酮输注后观察到BDNF增加时，24小时后观察到与dmPFC的断开，这可能反映了突触可塑性的影响。
{"title":"Ketamine-induced changes in plasma brain-derived neurotrophic factor (BDNF) levels are associated with the resting-state functional connectivity of the prefrontal cortex","authors":"Marie Woelfer, Meng Li, L. Colic, T. Liebe, Xin Di, B. Biswal, J. Murrough, V. Lessmann, T. Brigadski, M. Walter","doi":"10.1080/15622975.2019.1679391","DOIUrl":"https://doi.org/10.1080/15622975.2019.1679391","url":null,"abstract":"Abstract Objectives Synaptic plasticity and brain-derived neurotrophic factor (BDNF) signalling are proposed to play key roles in antidepressant drug action. Ketamine, an N-methyl-D-aspartate receptor antagonist and putative antidepressant, may increase synaptic plasticity in prefrontal cortex through higher expression of BDNF. Furthermore, ketamine was shown to change resting-state functional connectivity (RSFC) of dorsomedial prefrontal cortex (dmPFC). Methods In a randomised, placebo-controlled study, we investigated acutely (100 min) and at 24 h following subanesthetic ketamine infusion which dmPFC seeded RSFC changes are most strongly associated with plasma BDNF level changes in 53 healthy participants (21 females, age: 24.4 ± 2.9 years) using 7 T-fMRI. Results We observed higher relative levels of BDNF 2 h and 24 h after ketamine compared to placebo. Whole-brain regression revealed that the change in BDNF after 24 h was associated with RSFC decreases from dmPFC to posterior cingulate cortex and ventromedial PFC at 24 h and exploratively also at the 100 min measurement point. Follow-up analyses revealed that RSFC reductions following ketamine were restricted to subjects showing increased BDNF levels at 24 h. Conclusions Our findings indicate BDNF level dynamics following ketamine are related to acute and 24 h RSFC changes. Particularly when BDNF increases are observed after ketamine infusion, a disconnection from dmPFC after 24 h is seen and may reflect synaptic plasticity effects.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"169 1","pages":"696 - 710"},"PeriodicalIF":0.0,"publicationDate":"2020-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73151087","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 : 2020-05-27DOI: 10.1080/15622975.2019.1671609
S. Mitelman, M. Buchsbaum, B. Christian, Brian M. Merrill, B. Buchsbaum, J. Mukherjee, D. Lehrer
Abstract Objectives: Overlapping decreases in extrastriatal dopamine D2/D3-receptor availability and glucose metabolism have been reported in subjects with schizophrenia. It remains unknown whether these findings are physiologically related or coincidental. Methods: To ascertain this, we used two consecutive 18F-fluorodeoxyglucose and 18F-fallypride positron emission tomography scans in 19 healthy and 25 unmedicated schizophrenia subjects. Matrices of correlations between 18F-fluorodeoxyglucose uptake and 18F-fallypride binding in voxels at the same xyz location and AFNI-generated regions of interest were evaluated in both diagnostic groups. Results: 18F-fluorodeoxyglucose uptake and 18F-fallypride binding potential were predominantly positively correlated across the striatal and extrastriatal grey matter in both healthy and schizophrenia subjects. In comparison to healthy subjects, significantly weaker correlations in subjects with schizophrenia were confirmed in the right cingulate gyrus and thalamus, including the mediodorsal, lateral dorsal, anterior, and midline nuclei. Schizophrenia subjects showed decreased D2/D3-receptor availability in the hypothalamus, mamillary bodies, thalamus and several thalamic nuclei, and increased glucose uptake in three lobules of the cerebellar vermis. Conclusions: Dopaminergic system may be involved in modulation of grey matter metabolism and neurometabolic coupling in both healthy human brain and psychopathology. Hyperdopaminergic state in untreated schizophrenia may at least partly account for the corresponding decreases in grey matter metabolism.
{"title":"Positive association between cerebral grey matter metabolism and dopamine D2/D3 receptor availability in healthy and schizophrenia subjects: An 18F-fluorodeoxyglucose and 18F-fallypride positron emission tomography study","authors":"S. Mitelman, M. Buchsbaum, B. Christian, Brian M. Merrill, B. Buchsbaum, J. Mukherjee, D. Lehrer","doi":"10.1080/15622975.2019.1671609","DOIUrl":"https://doi.org/10.1080/15622975.2019.1671609","url":null,"abstract":"Abstract Objectives: Overlapping decreases in extrastriatal dopamine D2/D3-receptor availability and glucose metabolism have been reported in subjects with schizophrenia. It remains unknown whether these findings are physiologically related or coincidental. Methods: To ascertain this, we used two consecutive 18F-fluorodeoxyglucose and 18F-fallypride positron emission tomography scans in 19 healthy and 25 unmedicated schizophrenia subjects. Matrices of correlations between 18F-fluorodeoxyglucose uptake and 18F-fallypride binding in voxels at the same xyz location and AFNI-generated regions of interest were evaluated in both diagnostic groups. Results: 18F-fluorodeoxyglucose uptake and 18F-fallypride binding potential were predominantly positively correlated across the striatal and extrastriatal grey matter in both healthy and schizophrenia subjects. In comparison to healthy subjects, significantly weaker correlations in subjects with schizophrenia were confirmed in the right cingulate gyrus and thalamus, including the mediodorsal, lateral dorsal, anterior, and midline nuclei. Schizophrenia subjects showed decreased D2/D3-receptor availability in the hypothalamus, mamillary bodies, thalamus and several thalamic nuclei, and increased glucose uptake in three lobules of the cerebellar vermis. Conclusions: Dopaminergic system may be involved in modulation of grey matter metabolism and neurometabolic coupling in both healthy human brain and psychopathology. Hyperdopaminergic state in untreated schizophrenia may at least partly account for the corresponding decreases in grey matter metabolism.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"75 1","pages":"368 - 382"},"PeriodicalIF":0.0,"publicationDate":"2020-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80467989","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 : 2020-04-01DOI: 10.1080/15622975.2019.1648871
S. Mörkl, Daniel Seltenreich, M. Letmaier, S. Bengesser, W. Wurm, R. Grohmann, S. Bleich, S. Toto, S. Stübner, Mary I. Butler, S. Kasper
Abstract Objectives: Extrapyramidal symptoms (EPS) are a common adverse effect of antipsychotics. However, there are case reports describing EPS following treatment with antidepressants. It is not fully understood how antidepressants cause EPS, but a serotonergic input to dopaminergic pathways is a probable mechanism of action. Methods: Data from a multicenter drug-surveillance programme (AMSP, ‘drug safety in psychiatry’) which systemically documents severe drug reactions during psychiatric inpatient admissions, were reviewed to assess for EPS associated with antidepressant treatment. We identified 15 such cases, which were studied to detect similarities and to characterise risk factors. Results: We report on 15 patients with EPS following antidepressant-therapy between 1994 and 2016. EPS frequently occurred with selective serotonin reuptake inhibitor (SSRI) treatment alone (7/15 cases) or concomitant SSRI treatment (6/15 cases). EPS were most frequent with escitalopram-treatment (5 cases). The most common EPS was atypical dyskinesia (6/15 cases) followed by akathisia (4/15 cases). The mean age of onset for EPS was 54.93 years (SD 17.9). EPS occurred at any dosage and equally often in men and women. Conclusions: Our results highlight the possibility of EPS as an important, although uncommon, adverse effect of antidepressants. Clinicians should beware of this adverse effect and monitor early warning signs carefully.
{"title":"Extrapyramidal reactions following treatment with antidepressants: Results of the AMSP multinational drug surveillance programme","authors":"S. Mörkl, Daniel Seltenreich, M. Letmaier, S. Bengesser, W. Wurm, R. Grohmann, S. Bleich, S. Toto, S. Stübner, Mary I. Butler, S. Kasper","doi":"10.1080/15622975.2019.1648871","DOIUrl":"https://doi.org/10.1080/15622975.2019.1648871","url":null,"abstract":"Abstract Objectives: Extrapyramidal symptoms (EPS) are a common adverse effect of antipsychotics. However, there are case reports describing EPS following treatment with antidepressants. It is not fully understood how antidepressants cause EPS, but a serotonergic input to dopaminergic pathways is a probable mechanism of action. Methods: Data from a multicenter drug-surveillance programme (AMSP, ‘drug safety in psychiatry’) which systemically documents severe drug reactions during psychiatric inpatient admissions, were reviewed to assess for EPS associated with antidepressant treatment. We identified 15 such cases, which were studied to detect similarities and to characterise risk factors. Results: We report on 15 patients with EPS following antidepressant-therapy between 1994 and 2016. EPS frequently occurred with selective serotonin reuptake inhibitor (SSRI) treatment alone (7/15 cases) or concomitant SSRI treatment (6/15 cases). EPS were most frequent with escitalopram-treatment (5 cases). The most common EPS was atypical dyskinesia (6/15 cases) followed by akathisia (4/15 cases). The mean age of onset for EPS was 54.93 years (SD 17.9). EPS occurred at any dosage and equally often in men and women. Conclusions: Our results highlight the possibility of EPS as an important, although uncommon, adverse effect of antidepressants. Clinicians should beware of this adverse effect and monitor early warning signs carefully.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"83 1","pages":"308 - 316"},"PeriodicalIF":0.0,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83624619","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 : 2020-04-01DOI: 10.1080/15622975.2019.1679392
G. Joshi, M. DiSalvo, J. Wozniak, T. Ceranoglu, A. Yule, Craig B. H. Surman, R. Fried, M. Galdo, B. Hoskova, Abigail Belser, J. Biederman
Abstract Objectives: This treatment trial is aimed at assessing the short-term tolerability and efficacy of liquid-formulation extended-release methylphenidate (MPH-ER) for the treatment of attention deficit/hyperactivity disorder (ADHD) in adults with high-functioning autism spectrum disorder (HF-ASD). Methods: A 6-week open-label trial (ClinicalTrials.gov: NCT02096952) was conducted in 15 HF-ASD adults (mean age 24.9 ± 4.6; male, 12 (80%)) suffering from moderate-severe ADHD. MPH-ER was administered based on a flexible titration schedule. Efficacy was assessed on clinician- and self-rated measures. Tolerability was assessed by documenting treatment-emergent adverse events (AEs) and other safety measures. Results: Short-term MPH-ER treatment was associated with significant improvement in ADHD severity (Adult ADHD Investigator Symptom Report Scale (AISRS) mean change (MC), −22.8 ± 8.8, P < 0.001; Adult ADHD Self-Report Scale (ASRS) MC, −8.2 ± 15.3, P < 0.001). Twelve (80%) participants were deemed responders, based on ≥30% reduction in AISRS score and an ADHD Clinical Global Impression-Improvement score ≤2. MPH-ER was well-tolerated (treatment-limiting AEs, 1/15; severe AEs, 1/15) at mean dose of 48.7 ± 15 mg/day. AEs were transient and experienced by 13/15 (87%) participants at mild to moderate severity. Frequently reported AEs were as typically expected (headache (53%), insomnia (33%), anxiety (33%), decreased appetite (27%)). Conclusions: Our findings suggest that MPH-ER is effective and well-tolerated in the treatment of ADHD in HF-ASD adults.
{"title":"A prospective open-label trial of long-acting liquid methylphenidate for the treatment of attention deficit/hyperactivity disorder in intellectually capable adults with autism spectrum disorder","authors":"G. Joshi, M. DiSalvo, J. Wozniak, T. Ceranoglu, A. Yule, Craig B. H. Surman, R. Fried, M. Galdo, B. Hoskova, Abigail Belser, J. Biederman","doi":"10.1080/15622975.2019.1679392","DOIUrl":"https://doi.org/10.1080/15622975.2019.1679392","url":null,"abstract":"Abstract Objectives: This treatment trial is aimed at assessing the short-term tolerability and efficacy of liquid-formulation extended-release methylphenidate (MPH-ER) for the treatment of attention deficit/hyperactivity disorder (ADHD) in adults with high-functioning autism spectrum disorder (HF-ASD). Methods: A 6-week open-label trial (ClinicalTrials.gov: NCT02096952) was conducted in 15 HF-ASD adults (mean age 24.9 ± 4.6; male, 12 (80%)) suffering from moderate-severe ADHD. MPH-ER was administered based on a flexible titration schedule. Efficacy was assessed on clinician- and self-rated measures. Tolerability was assessed by documenting treatment-emergent adverse events (AEs) and other safety measures. Results: Short-term MPH-ER treatment was associated with significant improvement in ADHD severity (Adult ADHD Investigator Symptom Report Scale (AISRS) mean change (MC), −22.8 ± 8.8, P < 0.001; Adult ADHD Self-Report Scale (ASRS) MC, −8.2 ± 15.3, P < 0.001). Twelve (80%) participants were deemed responders, based on ≥30% reduction in AISRS score and an ADHD Clinical Global Impression-Improvement score ≤2. MPH-ER was well-tolerated (treatment-limiting AEs, 1/15; severe AEs, 1/15) at mean dose of 48.7 ± 15 mg/day. AEs were transient and experienced by 13/15 (87%) participants at mild to moderate severity. Frequently reported AEs were as typically expected (headache (53%), insomnia (33%), anxiety (33%), decreased appetite (27%)). Conclusions: Our findings suggest that MPH-ER is effective and well-tolerated in the treatment of ADHD in HF-ASD adults.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"60 1","pages":"274 - 290"},"PeriodicalIF":0.0,"publicationDate":"2020-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89021881","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 : 2020-03-01DOI: 10.1080/15622975.2019.1648870
D. Haleem, Sumera Gul
Abstract Objectives: To assess the role of circulating cortisol and leptin in depression associated with anorexia or obesity. Methods: Two hundred and fifty depressed patients presenting to the outpatient clinic of a psychiatric hospital and 250 non-depressed healthy volunteers were included in the study. The subjects of both groups were sub-grouped based upon their gender and BMI. Serum cortisol and leptin were determined by using respective ELISA kits. Results: The number of depressed than non-depressed subjects was three-fold higher in obese BMI groups of both genders. There were more depressed than non-depressed subjects in the underweight male BMI groups and in the overweight female BMI groups. There was a BMI-related increase in serum leptin and a decrease in serum cortisol in both genders. Depression in underweight BMI groups of both genders was associated with a decrease in serum leptin and an increase in cortisol. Higher serum leptin in obese BMI group was associated with a decrease in serum cortisol. Conclusions: Obesity is a risk factor for depression. The shift from typical to atypical depression is due to an inhibitory effect of higher circulating leptin on HPA axis activity and subsequent decrease in the lipolytic effects of cortisol.
{"title":"Circulating leptin, cortisol and gender differences associated with anorexia or obesity in depression","authors":"D. Haleem, Sumera Gul","doi":"10.1080/15622975.2019.1648870","DOIUrl":"https://doi.org/10.1080/15622975.2019.1648870","url":null,"abstract":"Abstract Objectives: To assess the role of circulating cortisol and leptin in depression associated with anorexia or obesity. Methods: Two hundred and fifty depressed patients presenting to the outpatient clinic of a psychiatric hospital and 250 non-depressed healthy volunteers were included in the study. The subjects of both groups were sub-grouped based upon their gender and BMI. Serum cortisol and leptin were determined by using respective ELISA kits. Results: The number of depressed than non-depressed subjects was three-fold higher in obese BMI groups of both genders. There were more depressed than non-depressed subjects in the underweight male BMI groups and in the overweight female BMI groups. There was a BMI-related increase in serum leptin and a decrease in serum cortisol in both genders. Depression in underweight BMI groups of both genders was associated with a decrease in serum leptin and an increase in cortisol. Higher serum leptin in obese BMI group was associated with a decrease in serum cortisol. Conclusions: Obesity is a risk factor for depression. The shift from typical to atypical depression is due to an inhibitory effect of higher circulating leptin on HPA axis activity and subsequent decrease in the lipolytic effects of cortisol.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"62 2 1","pages":"195 - 202"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79770178","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 : 2020-02-01DOI: 10.1080/15622975.2020.1757222
{"title":"Reviewers of the year 2019","authors":"","doi":"10.1080/15622975.2020.1757222","DOIUrl":"https://doi.org/10.1080/15622975.2020.1757222","url":null,"abstract":"","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"67 1","pages":"(i) - (i)"},"PeriodicalIF":0.0,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90927522","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 : 2019-12-10DOI: 10.1080/15622975.2019.1702717
M. Besse, M. Belz, T. Folsche, Jonathan Vogelgsang, I. Methfessel, P. Steinacker, M. Otto, J. Wiltfang, D. Zilles
Abstract Objectives: Although there is consistent evidence that electroconvulsive therapy (ECT) is safe and well tolerated by the majority of patients, some authors still accuse ECT to inevitably cause brain damage and permanent memory loss, assertions that may increase patients’ worries about a useful treatment. Recently, the measurement of neurofilament light chain (NFL) in peripheral blood was technically implemented, permitting longitudinal analysis of this biomarker for axonal damage. NFL is part of the axonal cytoskeleton and is released into the CSF and peripheral blood in the context of neuronal damage. Methods: In our study, blood from 15 patients with major depressive disorder receiving ECT was collected before the first ECT as well as 24 h and seven days after the last ECT, respectively. NFL concentrations were analysed using the ultrasensitive single molecule array (Simoa) technology. Results: NFL concentrations did not differ between patients and healthy controls, and there was no significant change in NFL levels in the course of ECT. On the contrary, we even found a slight decrease in absolute NFL concentrations. Conclusions: Our study confirms the safety of ECT by using a most sensitive method for the detection of NFL in peripheral blood as a biomarker of neuronal damage.
{"title":"Serum neurofilament light chain (NFL) remains unchanged during electroconvulsive therapy","authors":"M. Besse, M. Belz, T. Folsche, Jonathan Vogelgsang, I. Methfessel, P. Steinacker, M. Otto, J. Wiltfang, D. Zilles","doi":"10.1080/15622975.2019.1702717","DOIUrl":"https://doi.org/10.1080/15622975.2019.1702717","url":null,"abstract":"Abstract Objectives: Although there is consistent evidence that electroconvulsive therapy (ECT) is safe and well tolerated by the majority of patients, some authors still accuse ECT to inevitably cause brain damage and permanent memory loss, assertions that may increase patients’ worries about a useful treatment. Recently, the measurement of neurofilament light chain (NFL) in peripheral blood was technically implemented, permitting longitudinal analysis of this biomarker for axonal damage. NFL is part of the axonal cytoskeleton and is released into the CSF and peripheral blood in the context of neuronal damage. Methods: In our study, blood from 15 patients with major depressive disorder receiving ECT was collected before the first ECT as well as 24 h and seven days after the last ECT, respectively. NFL concentrations were analysed using the ultrasensitive single molecule array (Simoa) technology. Results: NFL concentrations did not differ between patients and healthy controls, and there was no significant change in NFL levels in the course of ECT. On the contrary, we even found a slight decrease in absolute NFL concentrations. Conclusions: Our study confirms the safety of ECT by using a most sensitive method for the detection of NFL in peripheral blood as a biomarker of neuronal damage.","PeriodicalId":22963,"journal":{"name":"The World Journal of Biological Psychiatry","volume":"9 1","pages":"148 - 154"},"PeriodicalIF":0.0,"publicationDate":"2019-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86905481","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 : 2019-11-22DOI: 10.1080/15622975.2019.1696475
R. von Känel, F. Merz, H. Pfister, T. Brückl, P. Zimmermann, M. Uhr, F. Holsboer, N. Höhne, M. Ising
Abstract Objectives Hypercoagulability is one mechanism to explain the increased risk of incident atherothrombotic disease in patients with major depressive disorder (MDD). We examined whether patients with remitted MDD show an enhanced procoagulant state. Methods 63 individuals (median age 35 years, 59% women), 40 with a DSM-IV diagnosis of remitted MDD, made by a clinical interview, and 23 healthy controls provided blood samples for the measurement of fibrinogen, D-dimer, von Willebrand factor, and plasminogen activator inhibitor-1. Standardised z-scores of plasma levels of these haemostatic factors were added to form a procoagulant index (PCI) as the primary outcome variable. Self-ratings of residual depressive symptoms and trait anxiety were also obtained. Results Compared with controls, remitted MDD patients had higher PCI (p = 0.013, Cohen’s d = 0.69) and fibrinogen (p = 0.001, d = 0.91), controlling for age, sex, body mass index, smoking and C-reactive protein. There were no significant associations of the PCI and individual haemostatic molecules with age of MDD onset, time since the last MDD episode, the number of previous MDD episodes and residual depressive symptoms. Additional adjustment for anxiety symptoms did not change these results. Conclusions Remitted MDD is associated with an enhanced procoagulant state. Hypercoagulability seems more a trait than a state characteristic of depression.
目的高凝是解释重度抑郁症(MDD)患者发生动脉粥样硬化性血栓形成疾病风险增加的一种机制。我们检查了MDD缓解的患者是否表现出增强的促凝状态。方法63例患者(中位年龄35岁，女性59%)，其中40例诊断为DSM-IV缓解型重度抑郁症，通过临床访谈，23例健康对照者提供血液样本，测定纤维蛋白原、d -二聚体、血管性血友病因子和纤溶酶原激活物抑制剂-1。这些止血因子的血浆水平的标准化z分数被加入形成促凝指数(PCI)作为主要结局变量。残余抑郁症状和特质焦虑的自我评定也被获得。结果与对照组相比，在控制年龄、性别、体重指数、吸烟和c反应蛋白的情况下，缓解型MDD患者PCI (p = 0.013, Cohen’s d = 0.69)和纤维蛋白原(p = 0.001, d = 0.91)均较高。PCI和个体止血分子与MDD发病年龄、上一次MDD发作时间、既往MDD发作次数和残留抑郁症状无显著相关性。对焦虑症状的额外调整并没有改变这些结果。结论:MDD缓解与促凝状态增强有关。高凝似乎更像是抑郁症的一种特征，而不是一种状态特征。
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