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Haroon, E., X. Chen, Z. Li, X. P. Hu, J. C. Felger e A. H. Miller. "Multimodal neural signature of inflammatory response in mood disorders". Brain, Behavior, and Immunity 66 (novembro de 2017): e38-e39. http://dx.doi.org/10.1016/j.bbi.2017.07.140.
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Moya, Gonzalo E., Phillip D. Rivera e Kristin E. Dittenhafer-Reed. "Evidence for the Role of Mitochondrial DNA Release in the Inflammatory Response in Neurological Disorders". International Journal of Molecular Sciences 22, n.º 13 (29 de junho de 2021): 7030. http://dx.doi.org/10.3390/ijms22137030.
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Mitochondria are regarded as the metabolic centers of cells and are integral in many other cell processes, including the immune response. Each mitochondrion contains numerous copies of mitochondrial DNA (mtDNA), a small, circular, and bacterial-like DNA. In response to cellular damage or stress, mtDNA can be released from the mitochondrion and trigger immune and inflammatory responses. mtDNA release into the cytosol or bloodstream can occur as a response to hypoxia, sepsis, traumatic injury, excitatory cytotoxicity, or drastic mitochondrial membrane potential changes, some of which are hallmarks of neurodegenerative and mood disorders. Released mtDNA can mediate inflammatory responses observed in many neurological and mood disorders by driving the expression of inflammatory cytokines and the interferon response system. The current understanding of the role of mtDNA release in affective mood disorders and neurodegenerative diseases will be discussed.
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Chang, Hui H., e Po S. Chen. "Inflammatory Biomarkers for Mood Disorders - A Brief Narrative Review". Current Pharmaceutical Design 26, n.º 2 (4 de março de 2020): 236–43. http://dx.doi.org/10.2174/1381612826666200115100726.
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Background: The nervous system and the immune system interact consistently in the brain and peripheries. Inflammation in the brain not only alters the metabolism of neurotransmitters, but also causes network dysfunction, structural changes, and the development of mood symptomology in patients with mood disorders. In addition, the dysregulation of the neuroimmune axis in mood disorders drives multiple-system comorbidities. Furthermore, patients with low-grade inflammation are more likely to exhibit treatment resistance with both pharmacotherapy and non-pharmacotherapy. Objective: The aim of this review was to examine the available data regarding not only evidence of inflammation in the pathophysiology of mood disorders and their comorbid conditions, but also potential inflammatory biomarkers of mood disorders. Methods: Studies of the use of adjunct anti-inflammatory medications in mood disorders, and inflammatory biomarkers that may guide treatment outcomes in mood disorders, were summarized. Results: Studies have demonstrated that certain adjunct anti-inflammatory medications might help to improve mood symptoms and reduce comorbidities, and the baseline levels of inflammatory biomarkers, such as peripheral C-reactive protein (CRP), could be used to stratify the treatment outcome. All results suggested that the identification of peripheral and brain inflammatory biomarkers for the diagnosis, outcome prediction, staging, and stratification of interventions of mood disorders has emerged as an important area of translational research in psychiatry. Conclusion: Inflammatory biomarkers could guide interventions and enhance treatment response in patients with mood disorders. The main challenge is that substantial complexities might hamper the attainment of this goal.
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Dominiak, Monika, Adam Gędek, Michalina Sikorska, Paweł Mierzejewski, Marcin Wojnar e Anna Z. Antosik-Wójcińska. "Acetylsalicylic Acid and Mood Disorders: A Systematic Review". Pharmaceuticals 16, n.º 1 (31 de dezembro de 2022): 67. http://dx.doi.org/10.3390/ph16010067.
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The effects of acetylsalicylic acid (ASA) on mood disorders (MD) and on inflammatory parameters in preclinical and clinical studies have not yet been comprehensively evaluated. The aim of this study was to systematically summarize the available knowledge on this topic according to PRISMA guidelines. Data from preclinical and clinical studies were analyzed, considering the safety and efficacy of ASA in the treatment of MD and the correlation of inflammatory parameters with the effect of ASA treatment. Twenty-one studies were included. Both preclinical and clinical studies found evidence indicating the safety and efficacy of low-dose ASA in the treatment of all types of affective episodes in MD. Observational studies have indicated a reduced risk of all types of affective episodes in chronic low-dose ASA users (HR 0.92, 95% CI:0.88, 0.95, p < 0.0001). An association between ASA response and inflammatory parameters was found in preclinical studies, but this was not confirmed in clinical trials. Further long-term clinical trials evaluating the safety and efficacy of ASA in recurrent MD, as well as assessing the linkage of ASA treatment with inflammatory phenotype and cytokines, are required. There is also a need for preclinical studies to understand the exact mechanism of action of ASA in MD.
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Bauer, Moisés E., e Antônio L. Teixeira. "Neuroinflammation in Mood Disorders: Role of Regulatory Immune Cells". Neuroimmunomodulation 28, n.º 3 (2021): 99–107. http://dx.doi.org/10.1159/000515594.
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Mood disorders are associated with chronic low-grade systemic (sterile) inflammation, with increased plasma levels of pro-inflammatory mediators targeting all tissues including the brain. Importantly<b>,</b> pro-inflammatory cytokines (ex., tumor-necrosis factor alpha [TNF-α], interleukin [IL]-6) regulate mood behavior and cognition by influencing neurotransmitter levels, activating stress-responsive endocrine axes, among other effects. However, the mechanisms underlying this enhanced inflammation are not well understood. There is increasing evidence indicating that impaired immunoregulatory mechanisms may play a role in this context. Patients with mood disorders (major depression [MDD] and bipolar disorder [BD]) have reduced numbers of major regulatory cells of both innate (natural killer regulatory cells and myeloid-derived suppressor cells [MDSCs]) and adaptive immune responses (CD4<sup>+</sup>CD25<sup>+</sup>FoxP3<sup>+</sup>, B regulatory cells). Dysfunctional regulatory immune cells might contribute to systemic and neuroinflammation observed in mood disorders via different mechanisms, such as: (i) failure to develop adequate stress-related responses, (ii) indirectly through microglial activation, (iii) lack of trophic support and pro-cognitive functions of T cells in the brain, and (iv) dysbiosis. In conclusion, maladaptive immunoregulatory mechanisms seem to be involved with both onset and progression of mood disorders. A deeper understanding of these mechanisms may lead to the development of new therapeutic strategies.
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Squassina, Alessio, Claudia Pisanu e Roberta Vanni. "Mood Disorders, Accelerated Aging, and Inflammation: Is the Link Hidden in Telomeres?" Cells 8, n.º 1 (15 de janeiro de 2019): 52. http://dx.doi.org/10.3390/cells8010052.
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Mood disorders are associated with an increased risk of aging-related diseases, which greatly contribute to the excess morbidity and mortality observed in affected individuals. Clinical and molecular findings also suggest that mood disorders might be characterized by a permanent state of low-grade inflammation. At the cellular level, aging translates into telomeres shortening. Intriguingly, inflammation and telomere shortening show a bidirectional association: a pro-inflammatory state seems to contribute to aging and telomere dysfunction, and telomere attrition is able to induce low-grade inflammation. Several independent studies have reported shorter telomere length and increased levels of circulating inflammatory cytokines in mood disorders, suggesting a complex interplay between altered inflammatory–immune responses and telomere dynamics in the etiopathogenesis of these disorders. In this review, we critically discuss studies investigating the role of telomere attrition and inflammation in the pathogenesis and course of mood disorders, and in pharmacological treatments with psychotropic medications.
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Silberstein, Susana, Ana Clara Liberman, Paula Ayelén dos Santos Claro, Maria Belén Ugo, Jan M. Deussing e Eduardo Arzt. "Stress-Related Brain Neuroinflammation Impact in Depression: Role of the Corticotropin-Releasing Hormone System and P2X7 Receptor". Neuroimmunomodulation 28, n.º 2 (2021): 52–60. http://dx.doi.org/10.1159/000515130.
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Depression and other psychiatric stress-related disorders are leading causes of disability worldwide. Up to date, treatments of mood disorders have limited success, most likely due to the multifactorial etiology of these conditions. Alterations in inflammatory processes have been identified as possible pathophysiological mechanisms in psychiatric conditions. Here, we review the main features of 2 systems involved in the control of these inflammatory pathways: the CRH system as a key regulator of the stress response and the ATP-gated ion-channel P2X7 receptor (P2X7R) involved in the control of immune functions. The pathophysiology of depression as a stress-related psychiatric disorder is depicted in terms of the impact of CRH and P2X7R function on inflammatory pathways in the brain. Understanding pathogenesis of affective disorders will lead to the development of therapies for treatment of depression and other stress-related diseases.
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Leite Dantas, Rafael, Jana Freff, Oliver Ambrée, Eva C. Beins, Andreas J. Forstner, Udo Dannlowski, Bernhard T. Baune, Stefanie Scheu e Judith Alferink. "Dendritic Cells: Neglected Modulators of Peripheral Immune Responses and Neuroinflammation in Mood Disorders?" Cells 10, n.º 4 (19 de abril de 2021): 941. http://dx.doi.org/10.3390/cells10040941.
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Affective disorders (AD) including major depressive disorder (MDD) and bipolar disorder (BD) are common mood disorders associated with increased disability and poor health outcomes. Altered immune responses characterized by increased serum levels of pro-inflammatory cytokines and neuroinflammation are common findings in patients with AD and in corresponding animal models. Dendritic cells (DCs) represent a heterogeneous population of myeloid cells that orchestrate innate and adaptive immune responses and self-tolerance. Upon sensing exogenous and endogenous danger signals, mature DCs secrete proinflammatory factors, acquire migratory and antigen presenting capacities and thus contribute to neuroinflammation in trauma, autoimmunity, and neurodegenerative diseases. However, little is known about the involvement of DCs in the pathogenesis of AD. In this review, we summarize the current knowledge on DCs in peripheral immune responses and neuroinflammation in MDD and BD. In addition, we consider the impact of DCs on neuroinflammation and behavior in animal models of AD. Finally, we will discuss therapeutic perspectives targeting DCs and their effector molecules in mood disorders.
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Saavedra, Juan M. "Angiotensin II AT1 receptor blockers as treatments for inflammatory brain disorders". Clinical Science 123, n.º 10 (23 de julho de 2012): 567–90. http://dx.doi.org/10.1042/cs20120078.
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The effects of brain AngII (angiotensin II) depend on AT1 receptor (AngII type 1 receptor) stimulation and include regulation of cerebrovascular flow, autonomic and hormonal systems, stress, innate immune response and behaviour. Excessive brain AT1 receptor activity associates with hypertension and heart failure, brain ischaemia, abnormal stress responses, blood–brain barrier breakdown and inflammation. These are risk factors leading to neuronal injury, the incidence and progression of neurodegerative, mood and traumatic brain disorders, and cognitive decline. In rodents, ARBs (AT1 receptor blockers) ameliorate stress-induced disorders, anxiety and depression, protect cerebral blood flow during stroke, decrease brain inflammation and amyloid-β neurotoxicity and reduce traumatic brain injury. Direct anti-inflammatory protective effects, demonstrated in cultured microglia, cerebrovascular endothelial cells, neurons and human circulating monocytes, may result not only in AT1 receptor blockade, but also from PPARγ (peroxisome-proliferator-activated receptor γ) stimulation. Controlled clinical studies indicate that ARBs protect cognition after stroke and during aging, and cohort analyses reveal that these compounds significantly reduce the incidence and progression of Alzheimer's disease. ARBs are commonly used for the therapy of hypertension, diabetes and stroke, but have not been studied in the context of neurodegenerative, mood or traumatic brain disorders, conditions lacking effective therapy. These compounds are well-tolerated pleiotropic neuroprotective agents with additional beneficial cardiovascular and metabolic profiles, and their use in central nervous system disorders offers a novel therapeutic approach of immediate translational value. ARBs should be tested for the prevention and therapy of neurodegenerative disorders, in particular Alzheimer's disease, affective disorders, such as co-morbid cardiovascular disease and depression, and traumatic brain injury.
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Gharipour, Mojgan, Majid Barekatain, Johoon Sung, Naghmeh Emami, Ladan Sadeghian, Minoo Dianatkhah, Nizal Sarrafzadegan e Shayesteh Jahanfar. "The Epigenetic Overlap between Obesity and Mood Disorders: A Systematic Review". International Journal of Molecular Sciences 21, n.º 18 (15 de setembro de 2020): 6758. http://dx.doi.org/10.3390/ijms21186758.
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(1) Background: Obesity and mood disorders are considered as the most prevalent morbidities in many countries. We suppose that epigenetic mechanisms may induce higher rates of obesity in subjects who suffer from mood disorders. In this systematic review, we focused on the potential roles of DNA methylation on mood disorders and obesity development. (2) Methods: This systematic review was conducted in accordance with the PRISMA statement and registered in Prospero. A systematic search was conducted in MEDLINE, Scopus, Web of Science, Cochrane Central database, EMBASE, and CINHAL. We also conducted a Grey literature search, such as Google Scholar. (3) Results: After deduplication, we identified 198 potentially related citations. Finally, ten unique studies met our inclusion criteria. We have found three overlap genes that show significant DNA methylation changes, both in obesity and depression. Pathway analysis interaction for TAPBP, BDNF, and SORBS2 confirmed the relation of these genes in both obesity and mood disorders. (4) Conclusions: While mechanisms linking both obesity and mood disorders to epigenetic response are still unknown, we have already known chronic inflammation induces a novel epigenetic program. As the results of gene enrichment, pathways analysis showed that TAPBP, BDNF, and SORBS2 linked together by inflammatory pathways. Hypermethylation in these genes might play a crucial rule in the co-occurrence of obesity and mood disorders.
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Pinto, S. L. Azevedo, R. Coelho e A. Silva. "Depression and multiple sclerosis–pathophysiological links: From biology to treatment". European Psychiatry 41, S1 (abril de 2017): S521—S522. http://dx.doi.org/10.1016/j.eurpsy.2017.01.691.
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IntroductionDepressive disorders (DD) are the second cause of disability worldwide. DD affect predominantly working age individuals, recurring in 75% of cases. DD pathophysiology is intricate and multi-factorial. Several inflammatory diseases have been linked to mood disorders. Amidst these conditions is multiple sclerosis (MS), a chronic inflammatory disease of the central nervous system, characterized by frequent exacerbations and progressive functional loss.ObjectiveTo review the current knowledge on DD and MS as comorbidities and the underlying pathophysiologic mechanisms.MethodsWe performed a bibliographic search in Pubmed–publications released in the last 5 years, written in English, Portuguese and Spanish, containing the keywords depression, inflammatory disorders, multiple sclerosis.ResultsThe inflammatory hypothesis of depression provides a strong foundation to explain its close link with multiple sclerosis. The incidence and prevalence of DD is significantly higher in MS, especially in men. Functional imaging studies have shown that depressive symptoms are closely linked to the extension of inflammatory lesions, especially on the frontal and parietal regions, with particular emphasis to those affecting the grey matter. On the one hand, the clinical course and response to treatment of MS may be hindered by DD; on the other hand, the evolution of MS lesions leads to fluctuations in mood, with significant improvement of DD with successful MS treatment, independently of physical improvement.ConclusionsThere appears to be a biological link between DD and MS, with a bidirectional interference in the clinical course, prognosis and treatment response. Thus, both conditions must be correctly identified and treated.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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Raison, Charles L. "Microglial Activation and Response to Anti-inflammatory Treatment in Major Depressive Disorder: Another Piece in the Inflammation–Mood Disorders Puzzle". Biological Psychiatry 88, n.º 8 (outubro de 2020): 594–96. http://dx.doi.org/10.1016/j.biopsych.2020.08.003.
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Herron, James, e Jonathan Cavanagh. "Inflammatory mechanisms of mental illness: brain inflammatory response to interferon stimulation". BJPsych Open 7, S1 (junho de 2021): S256. http://dx.doi.org/10.1192/bjo.2021.684.
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AimsWe hypothesise that peripheral IFN stimulation results in a brain inflammatory response via pathways of neuroimmune communication which in turn results in sickness-behaviour and depressive phenotype. We aim to determine if peripheral IFN stimulation results in brain inflammatory response including upregulation of inflammatory cytokines and chemokines.BackgroundThere is increasing interest in the role of dysregulated immune function and inflammation in the pathogenesis of psychiatric disorders including mood disorders and dementias. Immune mechanisms offer a new approach to investigating mechanism in addition to offering hope for new avenues of treatment.Interferon (IFN) therapy in humans is known to be associated with a significant risk of developing depression, both during therapy and increasing risk of relapse in the years following exposure, yet the mechanism remains unclear. IFN stimulation in animal models may offer insights into this phenomenon, in addition to furthering our understanding the role of immune mechanisms in the development of psychiatric phenotypes.MethodMice (n. 42) were exposed to either IFN-alpha, IFN-gamma or vehicle control using either osmotic pump or intraperitoneal injection over the course of 7 days. Mice were scarificed, brains were dissected and RNA extracted. Inflammatory gene transcription within the brain was determined using real time quantitative polymerase chain reaction (RTqPCR). Absolute quantification was achieved using standard curves and reference gene. Statistical significance was determined using Mann-Whitney or ANOVA/Kruskal-Wallis depending on normality of data and number of groups.ResultIFNγ stimulation is associated with a significant brain upregulation of a number of inflammatory cytokines and chemokines including Il1β, Tnfα, Il10, Ifnγ, Ccl2, Ccl5, Ccl19, Cxcl10 and Ccr5. However, unexpectedly we did not find IFNα stimulation to associate with brain inflammatory transcriptional changes.ConclusionThis work demonstrates a brain inflammatory response to peripheral IFNγ stimulation. The inflammatory profile, including upregulated chemokines, suggests that recruitment of leukocytes across the blood brain barrier may be part of the immune response. Further experiments using existing tissues will explore if there are structural/cellular changes within the brain parenchyma. Further experiments within the group will seek to demonstrate if IFN treatment associates with sickness behaviour in order to determine if this is a clinically meaningful model. Suprisingly, we did not see similar changes in the IFNα treated group, which requires further investigation.Funding: University of Glasgow, The Sackler Trust
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Fond, G. "Inflammation in psychiatric disorders". European Psychiatry 29, S3 (novembro de 2014): 551–52. http://dx.doi.org/10.1016/j.eurpsy.2014.09.347.
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One of the most promising research fields is the inflammatory component of major psychiatric diseases (depression, bipolar disorders and schizophrenia). Multiple recent reviews clearly demonstrate that depression, schizophrenia and bipolar disorder are associated with a dysregulation of immune responses as reflected by the observed abnormal profiles of circulating pro- and anti-inflammatory cytokines in affected patients. Considering the high rate of associated somatic comorbidity, major mental illnesses, especially bipolar disorders, have been proposed as multi-systemic inflammatory diseases affecting the brain as well as other organs. In parallel, chronic inflammatory diseases are known to have a high psychiatric comorbidity rate (especially with depression). The same overlap is also found in pharmacological drugs properties as several antidepressants (especially selective serotonin reuptake inhibitors), several antipsychotics and mood stabilizers have shown intrinsic anti-inflammatory properties [1,2]. We recently conducted a systematic review of the literature regarding the efficacy of anti-inflammatory drugs (classified according to their mechanisms of action) in MDD, schizophrenia and bipolar disorders) [3]. We found that polyunsaturated fatty acids (PUFAs) have anti-inflammatory properties and are effective in major depression with a good tolerance profile. One meta-analysis based on 5 trials indicated that COX-2 specific inhibitors showed effectiveness in schizophrenia. COX-1 inhibitors like low-dose aspirin may also have potential effectiveness in the three major disorders but further studies are warranted. Minocycline, an antibiotic that penetrates central nervous system, showed also effectiveness in schizophrenia. Anti-TNFalpha drugs showed important effectiveness in resistant depression with blood inflammatory abnormalities, but in only one randomized placebo-controlled trial [4]. However, in this trial, the anti-inflammatory drug was much more effective than classical antidepressants in patients with baseline elevated hs-CRP (a inflammatory marker).
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Asslih, Serena, Odeya Damri e Galila Agam. "Neuroinflammation as a Common Denominator of Complex Diseases (Cancer, Diabetes Type 2, and Neuropsychiatric Disorders)". International Journal of Molecular Sciences 22, n.º 11 (7 de junho de 2021): 6138. http://dx.doi.org/10.3390/ijms22116138.
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The term neuroinflammation refers to inflammation of the nervous tissue, in general, and in the central nervous system (CNS), in particular. It is a driver of neurotoxicity, it is detrimental, and implies that glial cell activation happens prior to neuronal degeneration and, possibly, even causes it. The inflammation-like glial responses may be initiated in response to a variety of cues such as infection, traumatic brain injury, toxic metabolites, or autoimmunity. The inflammatory response of activated microglia engages the immune system and initiates tissue repair. Through translational research the role played by neuroinflammation has been acknowledged in different disease entities. Intriguingly, these entities include both those directly related to the CNS (commonly designated neuropsychiatric disorders) and those not directly related to the CNS (e.g., cancer and diabetes type 2). Interestingly, all the above-mentioned entities belong to the same group of “complex disorders”. This review aims to summarize cumulated data supporting the hypothesis that neuroinflammation is a common denominator of a wide variety of complex diseases. We will concentrate on cancer, type 2 diabetes (T2DM), and neuropsychiatric disorders (focusing on mood disorders).
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Drexhage, H. A. "Changes in the Immune System and Gene Expression in Bipolar Disorder". European Psychiatry 24, S1 (janeiro de 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70520-6.
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The etiology of bipolar disorder is thought to involve multiple genes and environmental factors. Recently the immune system has been implicated in the pathogenesis. Various abnormalities indicate the presence of an activated inflammatory response system. In this presentation evidence will be presented on:1.A higher susceptibility for autoimmune diseases (thyroiditis, gastritis, type 1 diabetes), not only in patients but also in first degree relatives independent from mood disturbances.2.An inflammatory gene-expression signature comprising of 19 pro-inflammatory genes in monocytes, the monocyte (and its descendent cells) being important in the activation of the inflammatory response. The inflammatory gene-expression profile was also found in the monocytes of bipolar offspring, especially in those developing a mood disorder (prognostic value of the test?).3.Common environmental factors (infection, stress and dietary components?) as the factors causing the inflammatory monocyte gene-expression signature (evidenced in a twin study).4.A general T cell activation not only linked to the trait of the disorder, but also to the state of the disorder (i.e. with mania) and in part due to genetic factors (evidenced in a twin study). Also T cell activation is not linked to monocyte activation.5.A poor T regulator activation which is genetically determined and correlates with the presence of above-described autoimmune diseases.In sum, there is clear evidence for an activated inflammatory response system in bipolar disorder, yet different components are separately activated in a complex fashion linked to the phenotype of the disorder and involving both genes and environmental factors.
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Bernstein, Charles N. "Psychological Stress and Depression: Risk Factors for IBD?" Digestive Diseases 34, n.º 1-2 (2016): 58–63. http://dx.doi.org/10.1159/000442929.
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While it is widely accepted that chronic diseases such as inflammatory bowel disease (IBD) may trigger negative psychological emotions such as distress and even depression, it is unknown if this response to a chronic illness like IBD is solely a psychological response to an adverse situation or whether it also represents a biological response, that is, the active inflammatory state of IBD intersecting with the pathobiology of what mediates mood and anxiety disorders. There is a bi-directionality between psychological comorbidity and IBD with each influencing the course of the other when they coexist. Furthermore, there is much to learn in terms of the underlying pathobiology of depression and anxiety and how this may impact on the pathobiology of IBD. Several important questions in regards to psychological comorbidity and IBD will be reviewed in this chapter.
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Park, Hyun Jung, Sung Ja Rhie e Insop Shim. "Regulatory role of cytokines on etiology of depression in animal models: their biological mechanisms and clinical implication with physical exercise". Journal of Exercise Rehabilitation 18, n.º 6 (27 de dezembro de 2022): 344–49. http://dx.doi.org/10.12965/jer.2244506.253.
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It has been known that chronic psychological or physical stress elicits depressive behaviors (learned helplessness, anhedonia, anxiety, etc.) and also activates to release proinflammatory cytokines in the brain. Especially, postmenopausal women under stress condition exacerbates neuroimmune systems and mood disorder. Repeated restraint stress in the ovariectomized female rats poses an immune challenge which was capable of inducing depressive-like behaviors, promoting exaggerated corticosterone responses and changing the proinflammatory cytokine expression such as interleukin (IL)-1β in the brain. Also, anti-inflammatory cytokines including IL-4 are known to regulate inflammation caused by immune response or stress challenge. Furthermore, some studies reported that physical activity can reduce stress hormones and improve personal immunity. Physical exercise has been shown to be associated with decreased symptoms of depression and anxiety, and with improved physical health, immunological function, and psychological well-being. This paper aims to discuss an overview of how stress shapes neuroimmune response and diverse roles of cytokines in animals models, acting on depressive-like behavioral changes; some beneficial aspects of exercise on stress-related disorders are addressed.
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Scheggi, Simona, Graziano Pinna, Giulia Braccagni, Maria De Montis e Carla Gambarana. "PPARα Signaling: A Candidate Target in Psychiatric Disorder Management". Biomolecules 12, n.º 5 (20 de maio de 2022): 723. http://dx.doi.org/10.3390/biom12050723.
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Peroxisome proliferator-activator receptors (PPARs) regulate lipid and glucose metabolism, control inflammatory processes, and modulate several brain functions. Three PPAR isoforms have been identified, PPARα, PPARb/d, and PPARg, which are expressed in different tissues and cell types. Hereinafter, we focus on PPARα involvement in the pathophysiology of neuropsychiatric and neurodegenerative disorders, which is underscored by PPARα localization in neuronal circuits involved in emotion modulation and stress response, and its role in neurodevelopment and neuroinflammation. A multiplicity of downstream pathways modulated by PPARα activation, including glutamatergic neurotransmission, upregulation of brain-derived neurotrophic factor, and neurosteroidogenic effects, encompass mechanisms underlying behavioral regulation. Modulation of dopamine neuronal firing in the ventral tegmental area likely contributes to PPAR effects in depression, anhedonia, and autism spectrum disorder (ASD). Based on robust preclinical evidence and the initial results of clinical studies, future clinical trials should assess the efficacy of PPARα agonists in the treatment of mood and neurodevelopmental disorders, such as depression, schizophrenia, and ASD.
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Harsanyi, Stefan, Ida Kupcova, Lubos Danisovic e Martin Klein. "Selected Biomarkers of Depression: What Are the Effects of Cytokines and Inflammation?" International Journal of Molecular Sciences 24, n.º 1 (29 de dezembro de 2022): 578. http://dx.doi.org/10.3390/ijms24010578.
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Depression is one of the leading mental illnesses worldwide and lowers the quality of life of many. According to WHO, about 5% of the worldwide population suffers from depression. Newer studies report a staggering global prevalence of 27.6%, and it is rising. Professionally, depression belonging to affective disorders is a psychiatric illness, and the category of major depressive disorder (MDD) comprises various diagnoses related to persistent and disruptive mood disorders. Due to this fact, it is imperative to find a way to assess depression quantitatively using a specific biomarker or a panel of biomarkers that would be able to reflect the patients’ state and the effects of therapy. Cytokines, hormones, oxidative stress markers, and neuropeptides are studied in association with depression. The latest research into inflammatory cytokines shows that their relationship with the etiology of depression is causative. There are stronger cytokine reactions to pathogens and stressors in depression. If combined with other predisposing factors, responses lead to prolonged inflammatory processes, prolonged dysregulation of various axes, stress, pain, mood changes, anxiety, and depression. This review focuses on the most recent data on cytokines as markers of depression concerning their roles in its pathogenesis, their possible use in diagnosis and management, their different levels in bodily fluids, and their similarities in animal studies. However, cytokines are not isolated from the pathophysiologic mechanisms of depression or other psychiatric disorders. Their effects are only a part of the whole pathway.
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Fellendorf, Frederike T., Mirko Manchia, Alessio Squassina, Claudia Pisanu, Stefano Dall’Acqua, Stefania Sut, Sofia Nasini et al. "Is Poor Lithium Response in Individuals with Bipolar Disorder Associated with Increased Degradation of Tryptophan along the Kynurenine Pathway? Results of an Exploratory Study". Journal of Clinical Medicine 11, n.º 9 (29 de abril de 2022): 2517. http://dx.doi.org/10.3390/jcm11092517.
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Bipolar disorder is associated with an inflammation-triggered elevated catabolism of tryptophan to the kynurenine pathway, which impacts psychiatric symptoms and outcomes. The data indicate that lithium exerts anti-inflammatory effects by inhibiting indoleamine-2,3-dioxygenase (IDO)-1 activity. This exploratory study aimed to investigate the tryptophan catabolism in individuals with bipolar disorder (n = 48) compared to healthy controls (n = 48), and the associations with the response to mood stabilizers such as lithium, valproate, or lamotrigine rated with the Retrospective Assessment of the Lithium Response Phenotype Scale (or the Alda scale). The results demonstrate an association of a poorer response to lithium with higher levels of kynurenine, kynurenine/tryptophan ratio as a proxy for IDO-1 activity, as well as quinolinic acid, which, overall, indicates a pro-inflammatory state with a higher degradation of tryptophan towards the neurotoxic branch. The treatment response to valproate and lamotrigine was not associated with the levels of the tryptophan metabolites. These findings support the anti-inflammatory properties of lithium. Furthermore, since quinolinic acid has neurotoxic features via the glutamatergic pathway, they also strengthen the assumption that the clinical drug response might be associated with biochemical processes. The relationship between the lithium response and the measurements of the tryptophan to the kynurenine pathway is of clinical relevance and may potentially bring advantages towards a personalized medicine approach to bipolar disorder that allows for the selection of the most effective mood-stabilizing drug.
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Ravi, Meghna, Andrew H. Miller e Vasiliki Michopoulos. "The immunology of stress and the impact of inflammation on the brain and behaviour". BJPsych Advances 27, n.º 3 (5 de março de 2021): 158–65. http://dx.doi.org/10.1192/bja.2020.82.
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SUMMARYExposure to acute versus chronic stressors and threats activates the immune system in adaptive and maladaptive manners respectively. Chronic activation arising from persistent stress exposure can contribute to an inflammatory response in the periphery and in the brain that has been implicated in stress-related psychopathology, including depression and anxiety. We review the immunology of acute and chronic stress exposure, integrate this discussion with the emerging literature linking heightened immune activation and inflammation to mood and anxiety disorders, and consider the translational implications of the immune system's role in these psychiatric conditions, with a brief overview of potential interventions.
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Castro, L. C. "Depression and Cytokines: A Psychoneuroimmune Perspective". European Psychiatry 24, S1 (janeiro de 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70599-1.
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Background:Cytokine-induced sickness behaviour is an adaptative response to infection. Activation of the immune system, particularly the increased activity of several cytokines, has been implicated in the provocation or exacerbation of mood disorders.Aim:To discuss the relevance of psychoneuroimmunologic research in the understanding of the patophysiology and therapeutic targets of certain mental health disorders.Methods:Review of the literature. MEDLINE and PubMed databases searches for peer-reviewed studies, published between 2000 and 2008, using combinations of the Medline Subject Heading terms cytokines, sickness behaviour, immune system and depression, depressive illness.Results:Several lines of evidence support the relationship between cytokines and mood disorders. Cytokine elevations are more marked in severe depression and their activity may also relate with illness chronicity, neurovegetative features and high stress perception. It is argued that the activation of the inflammatory system, eliciting cytokine release and synthesis, provoke neuroendocrine and neurotransmitter changes, contributing to the development of depression. Some studies support that the brain cytokine system can become sensitized in response to non-immune stressors or to immune stressors occurring early in life.Discussion:The cytokines actions in the brain can help to clarify the patophysiology of certain psychiatric disorders, including depression. The research findings show an association between the activation of the brain cytokine system and depression, although the precise relationship between sickness behaviour and depression is still not clear. Further research in such a promising area of study is needed and can contribute to new therapeutical targets and a broader understanding of psychiatric disorders.
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Castro, L. C. "Depression and Cytokines: A Psychoneuroimmune Perspective". European Psychiatry 24, S1 (janeiro de 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70944-7.
Texto completo da fonteResumo:
Background:Cytokine-induced sickness behaviour is an adaptative response to infection. Activation of the immune system, particularly the increased activity of several cytokines, has been implicated in the provocation or exacerbation of mood disorders.Aim:To discuss the relevance of psychoneuroimmunologic research in the understanding of the patophysiology and therapeutic targets of certain mental health disorders.Methods:Review of the literature. MEDLINE and PubMed databases searches for peer-reviewed studies, published between 2000 and 2008, using combinations of the Medline Subject Heading terms cytokines, sickness behaviour, immune system and depression, depressive illness.Results:Several lines of evidence support the relationship between cytokines and mood disorders. Cytokine elevations are more marked in severe depression and their activity may also relate with illness chronicity, neurovegetative features and high stress perception. It is argued that the activation of the inflammatory system, eliciting cytokine release and synthesis, provoke neuroendocrine and neurotransmitter changes, contributing to the development of depression. Some studies support that the brain cytokine system can become sensitized in response to non-immune stressors or to immune stressors occurring early in life.Discussion:The cytokines actions in the brain can help to clarify the patophysiology of certain psychiatric disorders, including depression. The research findings show an association between the activation of the brain cytokine system and depression, although the precise relationship between sickness behaviour and depression is still not clear. Further research in such a promising area of study is needed and can contribute to new therapeutical targets and a broader understanding of psychiatric disorders.
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Primo de Carvalho Alves, Lucas, e Neusa Sica da Rocha. "Different cytokine patterns associate with melancholia severity among inpatients with major depressive disorder". Therapeutic Advances in Psychopharmacology 10 (janeiro de 2020): 204512532093792. http://dx.doi.org/10.1177/2045125320937921.
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Background Six melancholic features (MFs) of the Hamilton Depression Rating Scale (HAM-D6) represent the construct of melancholia along a continuum of severity (from least to most severe: depressed mood, work and activities, somatic symptoms, psychic anxiety, guilty feelings, psychomotor retardation). We aimed to evaluate the association between these MFs and inflammatory cytokines (IC) in the blood. Methods Each IC [interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), interleukin 2 (IL-2), IL-4, IL-6, IL-10, and IL-17] was associated with the HAM-D6 MFs of 139 severely depressed inpatients, using multiple linear regressions adjusted for covariates. Levels were compared with those of 100 healthy controls. Results Depressed mood was associated with higher levels of IL-4 ( β = 0.167; p = 0.041). Psychic anxiety: lower IL-17 levels ( β = –0.173; p = 0.039). Guilt feelings: lower IL-2 levels ( β = −0.168; p = 0.041) Psychomotor retardation: higher IL-6 levels ( β = 0.195; p = 0.017). Depressed patients’ TNF-α, INF-γ, and IL-4 levels were not significantly different from controls. Depressed patients’ IL-2, IL-6, IL-10, and IL-17 levels were higher than those of controls ( p <0.001). Conclusion Less severe MFs (depressed mood, psychic anxiety, and guilt feelings) were associated with an anti-inflammatory pattern (higher IL-4, lower IL-17 and lower IL-2, respectively). The presence of the most severe MF, psychomotor retardation, was associated with a higher pro-inflammatory response (higher IL-6).
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Ramirez DDS, MSc, PhD, Karol. "Neuroimmunological Responses to Social Isolation". Odovtos - International Journal of Dental Sciences 17, n.º 1 (29 de novembro de 2015): 10. http://dx.doi.org/10.15517/ijds.v0i0.22032.
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Objective social isolation and perceived social isolation are psychosocial stressors that may impair the normal functioning of the neuroimmune system. Chronic activation of the neuro-immuno-endocrine communication and the consequent loss of homeostasis may lead to the appearance of pathologies and associated mood disorders. For example, alterations in the hypothalamic-pituitary- adrenal axis and sympathetic nervous system dynamics may account for the observed predisposition to inflammatory diseases following chronic social stress. Therefore, it is necessary to further study the underlying mechanisms in social isolation in order to prevent its deleterious effects on health. The objective of this New Perspective article is to supplement the understanding of the neuroimmunological responses to social isolation and provide a basis for future research in this topic.
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Shalev, Hadar, Yonatan Serlin e Alon Friedman. "Breaching the Blood-Brain Barrier as a Gate to Psychiatric Disorder". Cardiovascular Psychiatry and Neurology 2009 (27 de agosto de 2009): 1–7. http://dx.doi.org/10.1155/2009/278531.
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The mechanisms underlying the development and progression of psychiatric illnesses are only partially known. Clinical data suggest blood-brain barrier (BBB) breakdown and inflammation are involved in some patients groups. Here we put forward the “BBB hypothesis” and abnormal blood-brain communication as key mechanisms leading to neuronal dysfunction underlying disturbed cognition, mood, and behavior. Based on accumulating clinical data and animal experiments, we propose that events within the “neurovascular unit” are initiated by a focal BBB breakdown, and are associated with dysfunction of brain astrocytes, a local inflammatory response, pathological synaptic plasticity, and increased network connectivity. Our hypothesis should be validated in animal models of psychiatric diseases and BBB breakdown. Recently developed imaging approaches open the opportunity to challenge our hypothesis in patients. We propose that molecular mechanisms controlling BBB permeability, astrocytic functions, and inflammation may become novel targets for the prevention and treatment of psychiatric disorders.
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Liu, Hua, Lian Lin Liu, Jing Chen, Yue Wen Chen, Yue Chai, Qing Shan Liu e Yong Cheng. "Muscone with Attenuation of Neuroinflammation and Oxidative Stress Exerts Antidepressant-Like Effect in Mouse Model of Chronic Restraint Stress". Oxidative Medicine and Cellular Longevity 2022 (30 de setembro de 2022): 1–10. http://dx.doi.org/10.1155/2022/3322535.
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Major depressive disorder (MDD) is a common mental disorder with high morbidity. Stress negatively affects for MDD development, whereby transport of stress-induced inflammatory mediators to the central nervous system (CNS) is associated with the etiology of mood disorders. Muscone is a pharmacologically active ingredient isolated from musk, with anti-inflammatory and neuroprotective effects. We hypothesized that muscone may ameliorate depression-like behavior by regulating inflammatory responses. To test this hypothesis, we used the chronic restraint stress (CRS) depression model, and CRS mice were treated with muscone (10 mg/kg, i.g., respectively) for 14 days. The effects of the drug on depressive-like behaviors were evaluated via the open field test (OFT), novelty-suppressed feeding test (NSFT), tail suspension test (TST), and forced swimming test (FST). Quantitative reverse transcription-PCR (qRT-PCR) was utilized to assess levels of proinflammatory cytokines (IL-6, TNF-α, COX2, and IL-1) and the anti-inflammatory cytokines (IL-4 and IL-10). We also determined levels of oxidative stress factors (malondialdehyde, superoxide dismutase, and glutathione peroxidase), as well as doublecortin (DCX) expression by immunofluorescence. The results showed that depression-like behavior and inflammatory levels were improved after muscone treatment. Muscone also significantly improved neurogenesis in the CRS mouse hippocampus and decreased oxidative stress in both the central and peripheral nervous systems. In conclusion, this work is the first to demonstrate that muscone has an antidepressant effect using a CRS model. Oxidative stress, neurogenesis, and inflammatory pathways are key factors affected by the drug and may represent new therapeutic targets to treat MDD, in this impact. These results may represent a new therapeutic target for MDD.
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Zhou, Feini, Hao Jiang, Ning Kong, Jiangnan Lin, Fan Zhang, Ting Mai, Zhijian Cao e Maosheng Xu. "Electroacupuncture Attenuated Anxiety and Depression-Like Behavior via Inhibition of Hippocampal Inflammatory Response and Metabolic Disorders in TNBS-Induced IBD Rats". Oxidative Medicine and Cellular Longevity 2022 (18 de janeiro de 2022): 1–19. http://dx.doi.org/10.1155/2022/8295580.
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This study was designed to explore the potential mechanisms of electroacupuncture (EA) in treating inflammatory bowel disease- (IBD-) related anxiety and mood disorders. A colitis model was induced in rats with 2, 4, 6-trinitrohydrosulfonic acid (TNBS), followed by ST36 and SP6 targeted therapy by EA or sham EA treatment. The elevated plus maze (EPM) and open-field test (OFT) were performed to assess the state of anxiety and depression-like behavior. Tests were carried out by 16S rDNA amplification sequence, 1H nuclear magnetic resonance (1H NMR) spectroscopy, immunofluorescence staining, and enzyme-linked immunosorbent assay (ELISA). The analyses detailed metabolic alterations and the Toll-like receptor 4 (TLR4) signaling pathway/NOD-like receptor protein 3 (NLRP3) inflammasome in rats’ hippocampal region. Furthermore, the activity of the hypothalamic-pituitary adrenal (HPA) axis and gut microbiome was assessed. As a result of treatment, EA significantly improved in the behavioral tests and altered the composition of the gut microbiome through a significant increase in the density of short chain fatty acids (SCFAs) producers mainly including Ruminococcaceae, Phascolarctobacterium, and Akkermansiaceae. EA upregulated the metabolites of the hippocampus mainly containing l-glutamine and gamma-aminobutyric acid (GABA), as well as ZO-1 expression. Whereas the treatment blocked the TLR4/nuclear factor- kappa B (NF-κB) signaling pathways and NLRP3 inflammasomes, along with downregulating the interleukin- (IL-) 1β level. The hyperactivity of the HPA axis was also diminished. In conclusion, EA at ST36 and SP6 attenuated anxiety and depression-like behavior in colitis model rats through their effects on the gut microbiome by modulating the hippocampal inflammatory response and metabolic disorders, as well as the HPA axis. This study provides evidence for clinical application of EA to serve as an adjunctive treatment for IBD-related anxiety and depression.
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Baj, Andreina, Elisabetta Moro, Michela Bistoletti, Viviana Orlandi, Francesca Crema e Cristina Giaroni. "Glutamatergic Signaling Along The Microbiota-Gut-Brain Axis". International Journal of Molecular Sciences 20, n.º 6 (25 de março de 2019): 1482. http://dx.doi.org/10.3390/ijms20061482.
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A complex bidirectional communication system exists between the gastrointestinal tract and the brain. Initially termed the “gut-brain axis” it is now renamed the “microbiota-gut-brain axis” considering the pivotal role of gut microbiota in maintaining local and systemic homeostasis. Different cellular and molecular pathways act along this axis and strong attention is paid to neuroactive molecules (neurotransmitters, i.e., noradrenaline, dopamine, serotonin, gamma aminobutyric acid and glutamate and metabolites, i.e., tryptophan metabolites), sustaining a possible interkingdom communication system between eukaryota and prokaryota. This review provides a description of the most up-to-date evidence on glutamate as a neurotransmitter/neuromodulator in this bidirectional communication axis. Modulation of glutamatergic receptor activity along the microbiota-gut-brain axis may influence gut (i.e., taste, visceral sensitivity and motility) and brain functions (stress response, mood and behavior) and alterations of glutamatergic transmission may participate to the pathogenesis of local and brain disorders. In this latter context, we will focus on two major gut disorders, such as irritable bowel syndrome and inflammatory bowel disease, both characterized by psychiatric co-morbidity. Research in this area opens the possibility to target glutamatergic neurotransmission, either pharmacologically or by the use of probiotics producing neuroactive molecules, as a therapeutic approach for the treatment of gastrointestinal and related psychiatric disorders.
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Trofimovitch, Diana, e Steven J. Baumrucker. "Pharmacology Update: Low-Dose Naltrexone as a Possible Nonopioid Modality for Some Chronic, Nonmalignant Pain Syndromes". American Journal of Hospice and Palliative Medicine® 36, n.º 10 (27 de março de 2019): 907–12. http://dx.doi.org/10.1177/1049909119838974.
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Pain can have a devastating effect on the quality of life of patients in palliative medicine. Thus far, majority of research has been centered on opioid-based pain management, with a limited empirical evidence for the use of nonopioid medications in palliative care. However, opioid and nonopioid medications such as nonsteroidal anti-inflammatory drugs have their limitations in the clinical use due to risk of adverse effects, therefore, there is a need for more research to be directed to finding an alternative approach to pain management in comfort care setting. The purpose of this article is to discuss a potential new drug that would adequately alleviate pain and enhance quality of life without significant risks of adverse effects that would limit its use. Naltrexone is a reversible competitive antagonist at μ-opioid and κ-opioid receptors, which when used at standard doses of 50 to 150 mg was initially intended for use in opioid and alcohol use disorders. However, it was discovered that its use in low doses follows alternate pharmacodynamic pathways with various effects. When used in doses of 1 to 5 mg it acts as a glial modulator with a neuroprotective effect via inhibition of microglial activation. It binds to Toll-like receptor 4 and acts as an antagonist, therefore inhibiting the downstream cellular signaling pathways that ultimately lead to pro-inflammatory cytokines, therefore reducing inflammatory response. Its other mode of action involves transient opioid receptor blockade ensuing from low-dose use which upregulates opioid signaling resulting in increased levels of endogenous opioid production, known as opioid rebound effect. Low dose naltrexone has gained popularity as an off-label treatment of several autoimmune diseases including multiple sclerosis and inflammatory bowel disease, as well as chronic pain disorders including fibromyalgia, complex regional pain syndrome, and diabetic neuropathy. Low-dose naltrexone (LDN) may also have utility in improving mood disorders and the potential to enhance the quality of life. This article will therefore propose the potential off-label use of LDN in management of nonmalignant pain in the palliative medicine setting.
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Xu, Tingting, Chunfang Liu, Xiulian Zhang, Lin Geng, Hongwei Wang, Li Li e Shengliang Zhu. "Network Pharmacology-Based Exploration of the Mechanism of Action of Shugan Hewei Recipe in the Treatment of Gastroesophageal Reflux Disease with Anxiety and Depression". Evidence-Based Complementary and Alternative Medicine 2022 (27 de setembro de 2022): 1–14. http://dx.doi.org/10.1155/2022/3957084.
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The Shugan Hewei recipe (SHR) is a well-recognized traditional Chinese medicine (TCM) prescription that has been shown to significantly improve chest pain, acid regurgitation, and the mood of GERD. Nonetheless, the underlying mechanisms remain unclear. In this study, the active compounds and targets of SHR were predicted using network pharmacology. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were utilized to explore the therapeutic mechanism of SHR. Combined with the drug target obtained from network pharmacology, the therapeutic effect and mechanism of SHR were observed. SHR’s main active compounds included quercetin, kaempferol, and luteolin. The core targets of SHR and GERD were TGF-β1, IL-1β, IL-4, CXCL10, MAPK1, MAPK3, CXCL8, IL-10, IL-2, and FOS, involving virus infection, inflammatory response, and body immunity. The core targets of SHR during the treatment of mental disorders were GABRA1, GABRA2, GABRA3, GABRA5, and GABRA6, involving synaptic transmission and transmembrane movement. Animal experiments revealed that SHR could repair the lower esophageal mucosa, mediate inflammatory factors, and GABA receptors and improve the behavior of rats. Overall, our results substantiate that SHR has huge prospects for widespread application in treating GERD subjects with anxiety and depression.
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Yoda, Kazutoyo, Gaku Harata, Mizuho Sato, Kenji Miyazawa, Natsuki Ohsawa, Fang He e Atsushi Toyoda. "Effect of Probiotic Bifidobacterium bifidum TMC3115 Supplementation on Psychosocial Stress Using a Sub-Chronic and Mild Social Defeat Stress in Mice". Nutrients 14, n.º 5 (24 de fevereiro de 2022): 970. http://dx.doi.org/10.3390/nu14050970.
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With the accumulation of knowledge on the relation between psychological stress and gut microbiota, there is growing interest in controlling stress and/or mood disorders via probiotic supplementation. We aimed to examine the effect of probiotic Bifidobacterium bifidum TMC3115 (TMC3115) supplementation using a sub-chronic and mild social defeat stress murine model in this study. TM3115 supplementation maintained body weight gain and alleviated a polydipsia-like symptom induced by the stress. In the analyses of fecal and cecal bacterial profiles, expansions of Proteobacteria in stressed mice and increases in Actinobacteria and Bifidobacterium in mice supplemented with TMC3115 were observed. There was no marked difference in the diversity of cecal bacteria between the tested mice. Elevated serum levels of inflammatory markers such as tumor necrosis factor (TNF)-α and interleukin (IL)-6 were observed in the stressed mice, while TMC3115 only reduced the IL-6 level. These findings suggest that TMC3115 supplementation confers tolerance to psychosocial stress in the host through modulation of the gut microbiota and alleviation of stress-induced inflammatory responses. Furthermore, it may be expected to exert prevention and treatment of disorders related to peripheral IL-6, including depression.
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Banfi, Davide, Elisabetta Moro, Annalisa Bosi, Michela Bistoletti, Silvia Cerantola, Francesca Crema, Fabrizio Maggi, Maria Cecilia Giron, Cristina Giaroni e Andreina Baj. "Impact of Microbial Metabolites on Microbiota–Gut–Brain Axis in Inflammatory Bowel Disease". International Journal of Molecular Sciences 22, n.º 4 (5 de fevereiro de 2021): 1623. http://dx.doi.org/10.3390/ijms22041623.
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The complex bidirectional communication system existing between the gastrointestinal tract and the brain initially termed the “gut–brain axis” and renamed the “microbiota–gut–brain axis”, considering the pivotal role of gut microbiota in sustaining local and systemic homeostasis, has a fundamental role in the pathogenesis of Inflammatory Bowel Disease (IBD). The integration of signals deriving from the host neuronal, immune, and endocrine systems with signals deriving from the microbiota may influence the development of the local inflammatory injury and impacts also more distal brain regions, underlying the psychophysiological vulnerability of IBD patients. Mood disorders and increased response to stress are frequently associated with IBD and may affect the disease recurrence and severity, thus requiring an appropriate therapeutic approach in addition to conventional anti-inflammatory treatments. This review highlights the more recent evidence suggesting that alterations of the microbiota–gut–brain bidirectional communication axis may concur to IBD pathogenesis and sustain the development of both local and CNS symptoms. The participation of the main microbial-derived metabolites, also defined as “postbiotics”, such as bile acids, short-chain fatty acids, and tryptophan metabolites in the development of IBD-associated gut and brain dysfunction will be discussed. The last section covers a critical evaluation of the main clinical evidence pointing to the microbiome-based therapeutic approaches for the treatment of IBD-related gastrointestinal and neuropsychiatric symptoms.
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Cojocariu, Roxana, Alin Ciobica, Ioana-Miruna Balmus, Samson Guenne, Anca Trifan, Carol Stanciu, Luminita Hrițcu e Radu Lefter. "Antioxidant Capacity and Behavioral Relevance of a Polyphenolic Extract of Chrysanthellum americanum in a Rat Model of Irritable Bowel Syndrome". Oxidative Medicine and Cellular Longevity 2019 (14 de agosto de 2019): 1–13. http://dx.doi.org/10.1155/2019/3492767.
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Chrysanthellum americanum L. (Vatke) is a medicinal plant from the Compositae family used in west-African traditional medicine, known for its flavonoid and saponin richness and for its strong antioxidant potential. In the present study, we assessed the effects of Chrysanthellum americanum polyphenolic extract in the psychological stress-induced rat model of irritable bowel syndrome (IBS), a chronic functional digestive tract disorder marked by immune and inflammatory-related disturbances of central nervous and peripheral intestinal systems, which is often associated with mood disorders including depression and anxiety. Consequently, memory impairment, anxiety and depression behavioral indicators, and cerebral oxidative stress biomarker dynamics were evaluated in a multifactorial heterotypic stress-exposed IBS rats after 6-day gavage with polyphenolic C. americanum extract (100 mg/kg body weight). Y-maze, elevated plus maze, and forced swimming tests were used for assessing behavioral responses. Administration of the extract exhibited significant anxiolytic and antidepressant-like effects coupled with significantly increased temporal lobe antioxidant enzyme specific activity (superoxide dismutase and glutathione peroxidase) and decreased malondialdehyde levels, a well-known lipid peroxidation marker. Furthermore, linear regression statistical analyses showed significant correlations between the oxidative stress parameters and behavioral tests. In conclusion, our results suggest that the administration of Chrysanthellum americanum polyphenolic extract could ameliorate mood and cognitive disturbances related to stress-induced in an IBS rat model. This could be also related to cerebral oxidative stress status attenuation.
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De Berardis, Domenico, Michele Fornaro, Alessandro Valchera, Marilde Cavuto, Giampaolo Perna, Marco Di Nicola, Gianluca Serafini et al. "Eradicating Suicide at Its Roots: Preclinical Bases and Clinical Evidence of the Efficacy of Ketamine in the Treatment of Suicidal Behaviors". International Journal of Molecular Sciences 19, n.º 10 (23 de setembro de 2018): 2888. http://dx.doi.org/10.3390/ijms19102888.
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Despite the continuous advancement in neurosciences as well as in the knowledge of human behaviors pathophysiology, currently suicide represents a puzzling challenge. The World Health Organization (WHO) has established that one million people die by suicide every year, with the impressive daily rate of a suicide every 40 s. The weightiest concern about suicidal behavior is how difficult it is for healthcare professionals to predict. However, recent evidence in genomic studies has pointed out the essential role that genetics could play in influencing person’s suicide risk. Combining genomic and clinical risk assessment approaches, some studies have identified a number of biomarkers for suicidal ideation, which are involved in neural connectivity, neural activity, mood, as well as in immune and inflammatory response, such as the mammalian target of rapamycin (mTOR) signaling. This interesting discovery provides the neurobiological bases for the use of drugs that impact these specific signaling pathways in the treatment of suicidality, such as ketamine. Ketamine, an N-methyl-d-aspartate glutamate (NMDA) antagonist agent, has recently hit the headlines because of its rapid antidepressant and concurrent anti-suicidal action. Here we review the preclinical and clinical evidence that lay the foundations of the efficacy of ketamine in the treatment of suicidal ideation in mood disorders, thereby also approaching the essential question of the understanding of neurobiological processes of suicide and the potential therapeutics.
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Recourt, Kasper, Jasper van der Aart, Gabriel Jacobs, Marieke de Kam, Wayne Drevets, Luc van Nueten, Kawita Kanhai et al. "Characterisation of the pharmacodynamic effects of the P2X7 receptor antagonist JNJ-54175446 using an oral dexamphetamine challenge model in healthy males in a randomised, double-blind, placebo-controlled, multiple ascending dose trial". Journal of Psychopharmacology 34, n.º 9 (4 de abril de 2020): 1030–42. http://dx.doi.org/10.1177/0269881120914206.
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Background: This is the first report of the pharmacodynamic (PD) effects of the selective, potent and brain-penetrant P2X7 receptor (P2X7R) antagonist JNJ-54175446. Activation of the P2X7R, an adenosine triphosphate-gated ion channel, leads to the production of pro-inflammatory cytokines, which have been linked to neuroinflammation and play a role in the pathogenesis of mood disorders. Previous clinical studies with JNJ-54175446 demonstrated peripheral target engagement of JNJ-54175446 by assessing ex vivo lipopolysaccharide (LPS)-stimulated cytokine production. Blood–brain barrier penetration and a clear dose–receptor occupancy relationship was demonstrated using positron emission tomography. Aims: The objectives of this double-blind, placebo-controlled, translational study were to assess the safety and tolerability of administering multiple doses of JNJ-54175446 and to explore its PD effects using a dexamphetamine challenge. Methods: Subjects ( N = 64) were randomised to either JNJ-54175446 (50–450 mg; n = 48) or placebo ( n = 16) and underwent a baseline oral 20 mg dexamphetamine challenge followed by 11 consecutive days q.d. dosing with JNJ-54175446/placebo and a randomised crossover dexamphetamine/placebo challenge. Results: At all doses tested, JNJ-54175446 was well tolerated and suppressed the ex vivo LPS-induced release of cytokines. At doses ⩾100 mg, JNJ-54175446 attenuated dexamphetamine-induced increases in locomotion and enhanced the mood-elevating effects of dexamphetamine, suggesting that a dose that is approximately twice as high is needed to obtain a central PD response compared to the dose needed for maximum peripheral occupancy. Conclusion: Overall, the observed pharmacological profile of JNJ-54175446 in the dexamphetamine challenge paradigm is compatible with a potential mood-modulating effect.
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D'Mello, Charlotte, e Mark G. Swain. "Liver-brain inflammation axis". American Journal of Physiology-Gastrointestinal and Liver Physiology 301, n.º 5 (novembro de 2011): G749—G761. http://dx.doi.org/10.1152/ajpgi.00184.2011.
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It is becoming increasingly evident that peripheral organ-centered inflammatory diseases, including chronic inflammatory liver diseases, are associated with changes in central neural transmission that result in alterations in behavior. These behavioral changes include sickness behaviors, such as fatigue, cognitive dysfunction, mood disorders, and sleep disturbances. While such behaviors have a significant impact on quality of life, the changes within the brain and the communication pathways between the liver and the brain that give rise to changes in central neural activity are not fully understood. Traditionally, neural and humoral communication pathways have been described, with the three cytokines TNFα, IL-1β, and IL-6 receiving the most attention in mediating communication between the periphery and the brain, in the setting of peripheral inflammation. However, more recently, we described an immune-mediated communication pathway in experimentally induced liver inflammation whereby, in response to activation of resident immune cells in the brain (i.e., the microglia), peripheral circulating monocytes transmigrate into the brain, leading to development of sickness behaviors. These signaling pathways drive changes in behavior by altering central neurotransmitter systems. Specifically, changes in serotonergic and corticotropin-releasing hormone neurotransmission have been demonstrated and implicated in liver inflammation-associated sickness behaviors. Understanding how the liver communicates with the brain in the setting of chronic inflammatory liver diseases will help delineate novel therapeutic targets that can reduce the burden of symptoms in patients with liver disease.
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Bai, Xue, Gerard Batallé e Olga Pol. "The Anxiolytic and Antidepressant Effects of Diallyl Disulfide and GYY4137 in Animals with Chronic Neuropathic Pain". Antioxidants 10, n.º 7 (3 de julho de 2021): 1074. http://dx.doi.org/10.3390/antiox10071074.
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When neuropathic pain is maintained long term, it can also lead to the development of emotional disorders that are even more intense than pain perception and difficult to treat. Hydrogen sulfide (H2S) donors relieve chronic pain, but their effects on the associated mood disorders are not completely elucidated. We evaluated if treatment with DADS (diallyl disulfide) or GYY4137 (morpholin-4-ium 4-methoxyphenyl(morpholino) phosphinodithioate dichloromethane complex), two slow-releasing H2S donors, inhibits the anxiety- and depressive-like behaviors that concur with chronic neuropathic pain generated by sciatic nerve injury in mice. The modulatory role of these drugs in the inflammatory, apoptotic, and oxidative processes implicated in the development of the affective disorders was assessed. Our results revealed the anxiolytic, antidepressant, and antinociceptive properties of DADS and GYY4137 during neuropathic pain by inhibiting microglial activation and the up-regulation of phosphoinositide 3-kinase/phosphorylated protein kinase B and BAX in the amygdala (AMG) and/or periaqueductal gray matter (PAG). Both treatments also normalized and/or activated the endogenous antioxidant system, but only DADS blocked ERK 1/2 phosphorylation. Both H2S donors decreased allodynia and hyperalgesia in a dose-dependent manner by activating the Kv7 potassium channels and heme oxygenase 1 signaling pathways. This study provides evidence of the anxiolytic and antidepressant properties of DADS and GYY4137 during neuropathic pain and reveals their analgesic actions, suggesting that these therapeutic properties may result from the inhibition of the inflammatory, apoptotic, and oxidative responses in the AMG and/or PAG. These findings support the use of these treatments for the management of affective disorders accompanying chronic neuropathic pain.
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Milano, Walter, Paola Ambrosio, Francesca Carizzone, Valeria De Biasio, Walter Di Munzio, Maria Gabriella Foia e Anna Capasso. "Depression and Obesity: Analysis of Common Biomarkers". Diseases 8, n.º 2 (14 de junho de 2020): 23. http://dx.doi.org/10.3390/diseases8020023.
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Depression and obesity are very common pathologies. Both cause significant problems of both morbidity and mortality and have decisive impacts not only on the health and well-being of patients, but also on socioeconomic and health expenditure aspects. Many epidemiological studies, clinical studies and meta-analyses support the association between mood disorders and obesity in relationships to different conditions such as the severity of depression, the severity of obesity, gender, socioeconomic status, genetic susceptibility, environmental influences and adverse experiences of childhood. Currently, both depression and obesity are considered pathologies with a high-inflammatory impact; it is believed that several overlapping factors, such as the activation of the cortico-adrenal axis, the exaggerated and prolonged response of the innate immune system and proinflammatory cytokines to stress factors and pathogens—as well as alterations of the intestinal microbiota which promote intestinal permeability—can favor the expression of an increasingly proinflammatory phenotype that can be considered a key and common phenomenon between these two widespread pathologies. The purpose of this literature review is to evaluate the common and interacting mechanisms between depression and obesity.
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Spichak, Simon, Timothy G. Dinan e John F. Cryan. "Gut–neuroimmune interactions: the unexpected role of the immune system in brain development". Biochemist 41, n.º 1 (1 de fevereiro de 2019): 36–41. http://dx.doi.org/10.1042/bio04101036.
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How does the immune system impact brain development? The exciting and somewhat unexpected relationship between the immune system and the brain has become one of the most fascinating topics in neuroscience. Even though the immune system was initially implicated in resolving viral and bacterial threats, it is now becoming more evident that it also plays a role in processes in the brain, both under healthy and pathological conditions. This novel role of the immune system in brain health has been implicated in various psychopathologies where neurodevelopment, stress and mood are central. In particular, its role in healthy brain development is becoming more evident, and understanding neuroimmune communication is becoming crucial in treating neurodevelopmental and mood disorders in later life. In the brain, glia function as part of the innate immune system and are programmed to respond to pathogens and physical injury. They also play an important role in neuronal development and pruning. These cells communicate with and respond to chemical signals, such as cytokines and chemokines, which can then initiate or downregulate inflammatory responses. Finally, the trillions of microbes residing in the gut can also stimulate cytokine and chemokine responses in the periphery and play an important role in both immunity and brain development.
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Fernandes, B. S., S. Dash, F. Jacka, S. Dodd, A. F. Carvalho, C. A. Köhler, J. Steiner et al. "Leptin in bipolar disorder: A systematic review and meta-analysis". European Psychiatry 35 (2016): 1–7. http://dx.doi.org/10.1016/j.eurpsy.2016.02.003.
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AbstractBackgroundBipolar disorder (BD) is a psychiatric disorder associated with increased rates of obesity and inflammation. Leptin is an adipokine that is mainly produced by the white adipose tissue in response to insulin. It stimulates the immune system, increasing the production of pro-inflammatory cytokines. There is currently uncertainty regarding possible alterations in peripheral leptin levels across the mood states in BD.MethodsThis study comprises a between-group meta-analysis comparing serum and plasma leptin levels in people with BD in mania, depression or euthymia and healthy controls. We conducted a systematic search for all possibly eligible-English and non-English peer-reviewed articles. We calculated the effect size (ES) utilizing Hedges’ adjusted g using random effects.ResultsEleven studies were included in the meta-analyses, providing data on 1118 participants. Serum and plasma leptin levels were not altered in subjects with BD when compared to healthy controls in mania (g = −0.99, 95% CI −2.43 to 0.43, P = 0.171), in depression (g = 0.17, 95% CI −0.45 to 0.79, P = 0.584), or in euthymia (g = 0.03, 95% CI −0.39 to 0.46, P = 0.882). However, we did observe a stronger association between leptin levels and both age and BMI in patients with BD in euthymia compared to healthy controls, such that the greater the age of the individuals, the greater the difference in leptin levels between BD and controls; and the higher the BMI, the greater the difference in leptin levels between BD and controls.ConclusionsOur meta-analysis provides evidence that leptin levels are not altered in BD across the mood spectrum compared to healthy controls. The disproportionate increase of leptin levels with increase in BMI in BD speaks in favour of a potential inflammatory role of white adipose tissue in BD and a disproportionate increase of leptin levels with increase in age.
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Kubick, Norwin, Marta Pajares, Ioana Enache, Gina Manda e Michel-Edwar Mickael. "Repurposing Zileuton as a Depression Drug Using an AI and In Vitro Approach". Molecules 25, n.º 9 (5 de maio de 2020): 2155. http://dx.doi.org/10.3390/molecules25092155.
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Repurposing drugs to target M1 macrophages inflammatory response in depression constitutes a bright alternative for commonly used antidepressants. Depression is a significant type of mood disorder, where patients suffer from pathological disturbances associated with a proinflammatory M1 macrophage phenotype. Presently, the most commonly used antidepressants such as Zoloft and Citalopram can reduce inflammation, but suffer from dangerous side effects without offering specificity toward macrophages. We employed a new strategy for drug repurposing based on the integration of RNA-seq analysis and text mining using deep neural networks. Our system employs a Google semantic AI universal encoder to compute sentences embedding. Sentences similarity is calculated using a sorting function to identify drug compounds. Then sentence relevance is computed using a custom-built convolution differential network. Our system highlighted the NRF2 pathway as a critical drug target to reprogram M1 macrophage response toward an anti-inflammatory profile (M2). Using our approach, we were also able to predict that lipoxygenase inhibitor drug zileuton could modulate NRF2 pathway in vitro. Taken together, our results indicate that reorienting zileuton usage to modulate M1 macrophages could be a novel and safer therapeutic option for treating depression.
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Ford, Bart, T. Kent Teague, Kyle Simmons, Martin Paulus e Jonathan Savitz. "Preliminary evidence of an interaction between sleep quality and inflammatory response on COVID19 vaccine immunogenicity in adults with a history of mood disorder". Brain, Behavior, and Immunity 106 (novembro de 2022): 2–3. http://dx.doi.org/10.1016/j.bbi.2022.07.019.
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Ragguett, Renee-Marie, Jocelyn K. Tamura e Roger S. McIntyre. "Keeping up with the clinical advances: depression". CNS Spectrums 24, S1 (28 de junho de 2019): 25–37. http://dx.doi.org/10.1017/s1092852919001159.
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Major depressive disorder (MDD) is a prevalent and heterogeneous disorder. Although there are many treatment options for MDD, patients with treatment-resistant depression (TRD) remain prevalent, wherein delayed time to response results in inferior chances of achieving remission. Recently, therapeutics have been developed that depart from the traditional monoamine hypothesis of depression and focus instead on the glutamatergic, GABAergic, opioidergic, and inflammatory systems. The literature suggests that the foregoing systems are implicated in the pathophysiology of MDD and preclinical trials have informed the development of pharmaceuticals using these systems as therapeutic targets. Pharmaceuticals that target the glutamatergic system include ketamine, esketamine, and rapastinel; brexanolone and SAGE-217 target the GABAergic system; minocycline targets the inflammatory system; and the combinatory agent buprenorphine + samidorphan targets the opioidergic system. The aforementioned agents have shown efficacy in treating MDD in clinical trials. Of particular clinical relevance are those agents targeting the glutamatergic and GABAergic systems as they exhibit rapid response relative to conventional antidepressants. Rapid response pharmaceuticals have the potential to transform the treatment of MDD, demonstrating reduction in depressive symptoms within 24 hours, as opposed to weeks noted with conventional antidepressants. Novel therapeutics have the potential to improve both patient mood symptomatology and economical productivity, reducing the debased human capital costs associated with MDD. Furthermore, a selection of therapeutic targets provides diverse treatment options which may be beneficial to the patient considering the heterogeneity of MDD.
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Szendi Md Habil, I., A. Bagi, S. Szalóki, E. Hallgató, N. Domján, A. Kanka, B. Gál et al. "Premorbid screening of healthy students may carry latent liability for schizophrenia or bipolar affective disorder with neurocognitive and neurophenomenological methods". European Psychiatry 65, S1 (junho de 2022): S683. http://dx.doi.org/10.1192/j.eurpsy.2022.1758.
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Introduction This study was carried out to map psychosis spectrum disorder risk factors. Objectives Our goal was to find what kind of instrumental methods may help to detect latent liabilities for schizophrenia and bipolar affective disorder Methods Using online questionnaires n=710 students were screened. Groups were formed based on the inclusion criteria: N = 25 people prone to mood swings, N = 30 people prone to odd experiences and delusive thinking, and a normal control group with N = 30 people. Personality, temperament, self-experiences, affectivity scales, and cognitive screening were conducted in addition to actigraphy coupled with a mobile application for detecting subjective experiences (EMA). Furthermore, instrumental examination of self-agency, testing time interval discrimination and (re)production, eye-tracking, EEG-microstates, and laboratory testing of inflammatory, immunologic and cardio-metabolic measures of allostatic load were applied. Results Self-experience disorders: both risk groups showed significantly higher scores than the control group (CG). Self-agency: based on incorrectly attributed responses, the positive schizotypy risk factor (PSF) group differed from the CG (p = 0.003). Antisaccade study: the PSF group showed a difference from the CG (p = 0.002). Actigraphy: based on the distributions of diurnal cumulative activities, it distinguished those with a cyclothymic risk factor (CTF) from the CG (67% probability in the k-means clustering procedure). Conclusions Healthy students with a latent liability for schizotypy or bipolarity could be distinguished by some targeted laboratory methods. Susceptibility for bipolarity was indicated by actigraphic analyzes, and the risk for schizotypal development was indicated by deficiencies in the self-agency experience and by anti-saccadic eye movement disorders. Disclosure No significant relationships.
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Anisman, Hymie. "Stress, immunity, cytokines and depression". Acta Neuropsychiatrica 14, n.º 6 (dezembro de 2002): 251–61. http://dx.doi.org/10.1034/j.1601-5215.2002.140601.x.
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The current issue of Acta Neuropsychiatrica presents a series of papers which together provide a broad overview relating stress, immunity, cytokine activity and depressive illness, as well as the influence of cytokines on other neurological disorders. This introduction to the issue presents a broad perspective of the impact of stressors on immune functioning in animal studies and in humans, considering the potential effects of acute, subchronic and chronic stressors, as well as the contribution of previous stressor experience in promoting neurochemical and immunological alterations. Given the supposition that cytokines may act as immunotransmitters, and immune challenge may be viewed as a stressor, a brief review is provided concerning the impact of stressors and cytokine challenges on central neurochemical functioning, with particular emphasis on the commonalties between the effects of these treatments. It is suggested that by virtue of the neurochemical changes imparted by cytokines, a depressive affect may be instigated, just as it is in response to psychogenic stressors. To this end, an overview is presented concerning the relationship between cytokines and depression, as well as the influence of cytokine treatments on behavioral changes in animal studies and among patients receiving immunotherapy. Provisionally, the data support the view that activation of the inflammatory response system may contribute to affective illness, and that cytokines may act as signaling molecules to activate central nervous system processes regulating mood states.
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WICHERS, M. C., G. H. KOEK, G. ROBAEYS, A. J. PRAAMSTRA e M. MAES. "Early increase in vegetative symptoms predicts IFN-α-induced cognitive-depressive changes". Psychological Medicine 35, n.º 3 (12 de novembro de 2004): 433–41. http://dx.doi.org/10.1017/s0033291704003526.
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Background. The vegetative symptoms of depression resemble the symptoms of malaise associated with activation of the inflammatory response system (IRS), and can be regarded as an expression of a central motivational state that resets the organism's priorities to promote recovery from infection. Early vegetative symptoms, however, may also contribute to the high rates of depression seen later in the course of immune activation. We hypothesized that the onset of vegetative-depressive symptoms early in the treatment with the pro-inflammatory cytokine IFN-α in chronic hepatitis C patients would increase the risk for subsequent depressive cognitions.Method. Sixteen patients eligible for IFN-α treatment and free of psychiatric disorders were recruited. The DSM-IV, the Multidimensional Fatigue Inventory, and the Montgomery–Asberg Depression Rating Scale (MADRS) were administered at baseline and 1, 2, 4, 8, 12 and 24 weeks after treatment was initiated. Cognitive-depressive and vegetative-depressive symptom clusters were constructed.Results. Fatigue and depression scores increased significantly during IFN-α treatment. Depression scores were highest at week 8 of treatment. First week increase in vegetative-depressive symptom score predicted cognitive-depressive symptom score at week 8 and at week 24.Conclusions. During IFN-α treatment, vegetative symptoms of depression appear earlier than, and are predictive of, their cognitive counterparts. This finding suggests that low mood state may in part be driven by the increase in early vegetative-depressive symptoms in the course of IFN-α-induced immune activation.
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Wang, Yu, Huili Jiang, Hong Meng, Jing Li, XinJing Yang, Bingcong Zhao, Yang Sun e Tuya Bao. "Antidepressant Mechanism Research of Acupuncture: Insights from a Genome-Wide Transcriptome Analysis of Frontal Cortex in Rats with Chronic Restraint Stress". Evidence-Based Complementary and Alternative Medicine 2017 (26 de setembro de 2017): 1–13. http://dx.doi.org/10.1155/2017/1676808.
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Major depressive disorder (MDD) is a chronic disease that adversely affects mood and cognition. In this study, we randomly divided the rats into control group (C), model group (M), fluoxetine group (F), and acupuncture group (A), used open-field test to ascertain whether acupuncture affects chronic restraint stress (CRS) induced depression-like behaviors of rats, and explored the antidepressant mechanism of acupuncture at the molecular level of transcriptome in the frontal cortex of CRS rats by RNA-sequencing (RNA-seq). According to differentially expressed genes (DEG) analysis, we identified 134, 46, and 89 response genes differentially expressed in C versus M, F versus M, and A versus M, respectively. Through Gene Ontology (GO) term enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, we identified the gene sets involved in extracellular space, inflammatory response, Toll-like receptor signaling pathway, chemokine signaling pathway, and TNF signaling pathway. In this study, RNA-seq technology was used to investigate the frontal cortex genome-wide transcriptomes in depression rats under CRS, which suggested that the antidepressant effect of acupuncture is effective and has a multitarget characteristic, which may be related to amino acid metabolism and inflammatory pathways, especially the Toll-like receptor signaling pathway, TNF signaling pathway, and NF-kappa B signaling pathway.
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Vani, Chiluvuru, e K. Srinivas Reddy. "PULSATILE DRUG DELIVERY SYSTEM-A TECHNIQUE OF DELIVERING DRUG IN ACCORDANCE WITH BIOLOGICAL CLOCK - A REVIEW". International Journal of Advanced Research 9, n.º 4 (30 de abril de 2021): 101–24. http://dx.doi.org/10.21474/ijar01/12813.
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Over last 30 years pulsatile drug delivery system has achieved a lot of importance in drug delivery technology. And the reason why this pulsatile drug delivery is gaining importance is because of its strategy of delivering drug molecule at right place, right time. There are certain diseases which are controlled by biological clock of our body and follow circadian rhythms like congestive heart failure, asthma, rheumatoid arthritis ,osteoarthritis, inflammatory disorders and other hormonal disorders, for this type of diseases conventional solid dosage forms like immediate release tablets or modified dosage forms like sustained, controlled release tablets cant give the required therapeutic response and also for such diseases delivering the drug at right time in right amount is very important. And that task is accomplished by this pulsatile drug delivery system. These pulsatile drug delivery framework is planned by the organic mood i.e., biological rhythms of the body, and medication conveyance is worked with by as per disease cadence. The rule for the utilization of pulsatile drug delivery of the medications is the place where a consistent drug discharge isnt wanted. The principle for the utilization of pulsatile release of the medications is the place where a steady drug discharge isnt wanted, yet drug release must be planned in such a way that, quick medication discharge is accomplished after the lag time. Current review examined the clarifications for improvement of pulsatile drug delivery framework in accordane with body circadian rhythm, kinds of the illness during which pulsatile discharge is required, order, assessments, benefits, impediments.