The Experts below are selected from a list of 253506 Experts worldwide ranked by ideXlab platform
Michael H. Silber - One of the best experts on this subject based on the ideXlab platform.
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Antidepressants increase rem sleep muscle tone in patients with and without rem sleep behavior disorder
Sleep, 2015Co-Authors: Stuart J Mccarter, St Louis Ek, David J Sandness, K Arndt, M Erickson, G Tabatabai, B F Boeve, Michael H. SilberAbstract:STUDY OBJECTIVES: REM sleep behavior disorder (RBD) is associated with Antidepressant treatment, especially in younger patients; but quantitative REM sleep without atonia (RSWA) analyses of psychiatric RBD patients remain limited. We analyzed RSWA in adults receiving Antidepressants, with and without RBD. DESIGN: We comparatively analyzed visual, manual, and automated RSWA between RBD and control groups. RSWA metrics were compared between groups, and regression was used to explore associations with clinical variables. SETTING: Tertiary-care sleep center. PARTICIPANTS: Participants included traditional RBD without Antidepressant treatment (n = 30, 15 Parkinson disease [PD-RBD] and 15 idiopathic); psychiatric RBD receiving Antidepressants (n = 30); and adults without RBD, including Antidepressant-treated psychiatric (n = 30), untreated psychiatric (n = 15), and OSA (n = 60) controls. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: RSWA was highest in traditional and psychiatric RBD, intermediate in treated psychiatric controls, and lowest in untreated psychiatric and OSA controls (P < 0.01). RSWA distribution and type also differed between Antidepressant-treated patients having higher values in anterior tibialis, and PD-RBD with higher submentalis and tonic RSWA. Psychiatric RBD had significantly younger age at onset than traditional RBD patients (P < 0.01). CONCLUSIONS: Antidepressant treatment was associated with elevated REM sleep without atonia (RSWA) even without REM sleep behavior disorder (RBD), suggesting that Antidepressants, not depression, promote RSWA. Differences in RSWA distribution and type were also seen, with higher anterior tibialis RSWA in Antidepressant-treated patients and higher tonic RSWA in Parkinson disease-RBD patients, which could aid distinction between RBD subtypes. These findings suggest that Antidepressants may mediate different RSWA mechanisms or, alternatively, that RSWA type and distribution evolve during progressive neurodegeneration. Further prospective RSWA analyses are necessary to clarify the relationships between Antidepressant treatment, psychiatric disease, and RBD.
Stephanie C. Dulawa - One of the best experts on this subject based on the ideXlab platform.
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Identifying fast-onset Antidepressants using rodent models
Molecular Psychiatry, 2017Co-Authors: M. J. Ramaker, Stephanie C. DulawaAbstract:Depression is a leading cause of disability worldwide and a major contributor to the burden of suicide. A major limitation of classical Antidepressants is that 2–4 weeks of continuous treatment is required to elicit therapeutic effects, prolonging the period of depression, disability and suicide risk. Therefore, the development of fast-onset Antidepressants is crucial. Preclinical identification of fast-onset Antidepressants requires animal models that can accurately predict the delay to therapeutic onset. Although several well-validated assay models exist that predict Antidepressant potential, few thoroughly tested animal models exist that can detect therapeutic onset. In this review, we discuss and assess the validity of seven rodent models currently used to assess Antidepressant onset: olfactory bulbectomy, chronic mild stress, chronic forced swim test, novelty-induced hypophagia (NIH), novelty-suppressed feeding (NSF), social defeat stress, and learned helplessness. We review the effects of classical Antidepressants in these models, as well as six treatments that possess fast-onset Antidepressant effects in the clinic: electroconvulsive shock therapy, sleep deprivation, ketamine, scopolamine, GLYX-13 and pindolol used in conjunction with classical Antidepressants. We also discuss the effects of several compounds that have yet to be tested in humans but have fast-onset Antidepressant-like effects in one or more of these Antidepressant onset sensitive models. These compounds include selective serotonin (5-HT) 2C receptor antagonists, a 5-HT 4 receptor agonist, a 5-HT 7 receptor antagonist, NMDA receptor antagonists, a TREK-1 receptor antagonist, mGluR antagonists and (2R,6R)-HNK. Finally, we provide recommendations for identifying fast-onset Antidepressants using rodent behavioral models and molecular approaches.
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requirement of hippocampal neurogenesis for the behavioral effects of Antidepressants
Science, 2003Co-Authors: Luca Santarelli, Stephanie C. Dulawa, Ronald S Duman, Michael Saxe, Cornelius Gross, Alexandre Surget, Fortunato Battaglia, Noelia V Weisstaub, Ottavio Arancio, Catherine BelzungAbstract:Various chronic Antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting Antidepressant-induced neurogenesis blocks behavioral responses to Antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of Antidepressants. These findings suggest that the behavioral effects of chronic Antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.
G Tabatabai - One of the best experts on this subject based on the ideXlab platform.
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Antidepressants increase rem sleep muscle tone in patients with and without rem sleep behavior disorder
Sleep, 2015Co-Authors: Stuart J Mccarter, St Louis Ek, David J Sandness, K Arndt, M Erickson, G Tabatabai, B F Boeve, Michael H. SilberAbstract:STUDY OBJECTIVES: REM sleep behavior disorder (RBD) is associated with Antidepressant treatment, especially in younger patients; but quantitative REM sleep without atonia (RSWA) analyses of psychiatric RBD patients remain limited. We analyzed RSWA in adults receiving Antidepressants, with and without RBD. DESIGN: We comparatively analyzed visual, manual, and automated RSWA between RBD and control groups. RSWA metrics were compared between groups, and regression was used to explore associations with clinical variables. SETTING: Tertiary-care sleep center. PARTICIPANTS: Participants included traditional RBD without Antidepressant treatment (n = 30, 15 Parkinson disease [PD-RBD] and 15 idiopathic); psychiatric RBD receiving Antidepressants (n = 30); and adults without RBD, including Antidepressant-treated psychiatric (n = 30), untreated psychiatric (n = 15), and OSA (n = 60) controls. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: RSWA was highest in traditional and psychiatric RBD, intermediate in treated psychiatric controls, and lowest in untreated psychiatric and OSA controls (P < 0.01). RSWA distribution and type also differed between Antidepressant-treated patients having higher values in anterior tibialis, and PD-RBD with higher submentalis and tonic RSWA. Psychiatric RBD had significantly younger age at onset than traditional RBD patients (P < 0.01). CONCLUSIONS: Antidepressant treatment was associated with elevated REM sleep without atonia (RSWA) even without REM sleep behavior disorder (RBD), suggesting that Antidepressants, not depression, promote RSWA. Differences in RSWA distribution and type were also seen, with higher anterior tibialis RSWA in Antidepressant-treated patients and higher tonic RSWA in Parkinson disease-RBD patients, which could aid distinction between RBD subtypes. These findings suggest that Antidepressants may mediate different RSWA mechanisms or, alternatively, that RSWA type and distribution evolve during progressive neurodegeneration. Further prospective RSWA analyses are necessary to clarify the relationships between Antidepressant treatment, psychiatric disease, and RBD.
Jacques Montplaisir - One of the best experts on this subject based on the ideXlab platform.
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Antidepressants and rem sleep behavior disorder isolated side effect or neurodegenerative signal
Sleep, 2013Co-Authors: Ronald B. Postuma, Jean-françois Gagnon, Veronique Latreille, Catherine Desjardins, Josieanne Bertrand, Maria Tuineaig, Jacques MontplaisirAbstract:OBJECTIVES Antidepressants, among the most commonly prescribed medications, trigger symptoms of REM sleep behavior disorder (RBD) in up to 6% of users. Idiopathic RBD is a very strong prodromal marker of Parkinson disease and other synuclein-mediated neurodegenerative syndromes. It is therefore critically important to understand whether Antidepressant-associated RBD is an independent pharmacologic syndrome or a sign of possible prodromal neurodegeneration. DESIGN Prospective cohort study. SETTING Tertiary sleep disorders center. PARTICIPANTS 100 patients with idiopathic RBD, all with diagnosis confirmed on polysomnography, stratified to baseline Antidepressant use, with 45 matched controls. MEASUREMENTS/RESULTS Of 100 patients, 27 were taking Antidepressants. Compared to matched controls, RBD patients taking Antidepressants demonstrated significant abnormalities of 12/14 neurodegenerative markers tested, including olfaction (P = 0.007), color vision (P = 0.004), Unified Parkinson Disease Rating Scale II and III (P < 0.001 and 0.007), timed up-and-go (P = 0.003), alternate tap test (P = 0.002), Purdue Pegboard (P = 0.007), systolic blood pressure drop (P = 0.029), erectile dysfunction (P = 0.002), constipation (P = 0.003), depression indices (P < 0.001), and prevalence of mild cognitive impairment (13% vs. 60%, P < 0.001). All these abnormalities were indistinguishable in severity from RBD patients not taking Antidepressants. However, on prospective follow-up, RBD patients taking Antidepressants had a lower risk of developing neurodegenerative disease than those without Antidepressant use (5-year risk = 22% vs. 59%, RR = 0.22, 95%CI = 0.06, 0.74). CONCLUSIONS Although patients with Antidepressant-associated RBD have a lower risk of neurodegeneration than patients with "purely-idiopathic" RBD, markers of prodromal neurodegeneration are still clearly present. Development of RBD with Antidepressants can be an early signal of an underlying neurodegenerative disease.
Benoit H Mulsant - One of the best experts on this subject based on the ideXlab platform.
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individual differences in response to Antidepressants a meta analysis of placebo controlled randomized clinical trials
JAMA Psychiatry, 2020Co-Authors: Marta M Maslej, Toshiaki A Furukawa, Andrea Cipriani, Paul W Andrews, Benoit H MulsantAbstract:Importance Antidepressants are commonly used worldwide to treat major depressive disorder. Symptomatic response to Antidepressants can vary depending on differences between individuals; however, this variability may reflect nonspecific or random factors. Objectives To investigate the assumption of systematic variability in symptomatic response to Antidepressants and to assess whether this variability is associated with severity of major depressive disorder, Antidepressant class, or year of study publication. Data Sources Data used were from a recent network meta-analysis of acute treatment with licensed Antidepressants in adults with major depressive disorder. The following databases were searched from inception to January 8, 2016: the Cochrane Central Register of Controlled Trials, CINAHL, Embase, LILACS database, MEDLINE, MEDLINE In-Process, and PsycINFO. Additional sources were international trial registries, drug approval agency websites, and key scientific journals. Study Selection Analysis was restricted to double-blind, randomized placebo-controlled trials with available data at the study’s end point. Data Extraction and Synthesis Baseline and end point means, SDs, number of participants in each group, Antidepressant class, and publication year were extracted. The data were analyzed between August 14 and November 18, 2019. Main Outcomes and Measures With the use of validated methods, coefficients of variation were derived for Antidepressants and placebo, and their ratios were calculated to compare outcome variability between Antidepressant and placebo. Ratios were entered into a random-effects model, with the expectation that response to Antidepressants would be more variable than response to placebo. Analysis was repeated after stratifying by baseline severity of depression, Antidepressant class (selective serotonin reuptake inhibitors: citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, and vilazodone; serotonin and norepinephrine reuptake inhibitors: desvenlafaxine and venlafaxine; norepinephrine-dopamine reuptake inhibitor: bupropion; noradrenergic agents: amitriptyline and reboxetine; and other Antidepressants: agomelatine, mirtazapine, and trazodone), and publication year. Results In the 87 eligible randomized placebo-controlled trials (17 540 unique participants), there was significantly more variability in response to Antidepressants than to placebo (coefficients of variation ratio, 1.14; 95% CI, 1.11-1.17;P Conclusions and Relevance Individual differences may be systematically associated with responses to Antidepressants in major depressive disorder beyond placebo effects or statistical factors. This study provides empirical support for identifying moderators and personalizing Antidepressant treatment.