Bibliografias temáticas / Neurobiology of mood disorders

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Literatura científica selecionada sobre o tema "Neurobiology of mood disorders"

Autor: Grafiati

Publicado: 14 de março de 2023

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Artigos de revistas sobre o assunto "Neurobiology of mood disorders"

Sullivan, John L. "Neurobiology of Mood Disorders". Psychosomatics 26, n.º 6 (junho de 1985): 553–54. http://dx.doi.org/10.1016/s0033-3182(85)72842-3.

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DUNNER, DAVID L. "Neurobiology of Mood Disorders". American Journal of Psychiatry 142, n.º 1 (janeiro de 1985): 135—a—135. http://dx.doi.org/10.1176/ajp.142.1.135-a.

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Rubin, Eugene H., e Charles F. Zorumski. "Neurobiology of Mood Disorders". Journal of Nervous and Mental Disease 173, n.º 2 (fevereiro de 1985): 126. http://dx.doi.org/10.1097/00005053-198502000-00013.

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Charney, D. S. "The Neurobiology of Mood Disorders". Archives of Neurology 59, n.º 2 (1 de fevereiro de 2002): 326—a—326. http://dx.doi.org/10.1001/archneur.59.2.326-a.

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Pande, Atul C., e Paul Max. "Book Review: Neurobiology of Mood Disorders". Canadian Journal of Psychiatry 31, n.º 7 (outubro de 1986): 693–94. http://dx.doi.org/10.1177/070674378603100721.

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Frazier, Jean A., e Jair C. Soares. "Neurobiology of Pediatric Mood Disorders: Part II". Journal of Child and Adolescent Psychopharmacology 19, n.º 1 (fevereiro de 2009): 1–2. http://dx.doi.org/10.1089/cap.2009.1911.

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Emery, Michael A., e Huda Akil. "Endogenous Opioids at the Intersection of Opioid Addiction, Pain, and Depression: The Search for a Precision Medicine Approach". Annual Review of Neuroscience 43, n.º 1 (8 de julho de 2020): 355–74. http://dx.doi.org/10.1146/annurev-neuro-110719-095912.

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Opioid addiction and overdose are at record levels in the United States. This is driven, in part, by their widespread prescription for the treatment of pain, which also increased opportunity for diversion by sensation-seeking users. Despite considerable research on the neurobiology of addiction, treatment options for opioid abuse remain limited. Mood disorders, particularly depression, are often comorbid with both pain disorders and opioid abuse. The endogenous opioid system, a complex neuromodulatory system, sits at the neurobiological convergence point of these three comorbid disease states. We review evidence for dysregulation of the endogenous opioid system as a mechanism for the development of opioid addiction and/or mood disorder. Specifically, individual differences in opioid system function may underlie differences in vulnerability to opioid addiction and mood disorders. We also review novel research, which promises to provide more detailed understanding of individual differences in endogenous opioid neurobiology and its contribution to opioid addiction susceptibility.

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Syed, Shariful A., e Charles B. Nemeroff. "Early Life Stress, Mood, and Anxiety Disorders". Chronic Stress 1 (fevereiro de 2017): 247054701769446. http://dx.doi.org/10.1177/2470547017694461.

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Early life stress has been shown to exert profound short- and long-term effects on human physiology both in the central nervous system and peripherally. Early life stress has demonstrated clear association with many psychiatric disorders including major depression, posttraumatic stress disorder, and bipolar disorder. The Diagnostic and Statistics Manuel of Mental Disorders (DSM) diagnostic categorical system has served as a necessary framework for clinical service, delivery, and research, however has not been completely matching the neurobiological research perspective. Early life stress presents a complex dynamic featuring a wide spectrum of physiologic alterations: from epigenetic alterations, inflammatory changes, to dysregulation of the hypothalamic pituitary axis and has further added to the challenge of identifying biomarkers associated with psychiatric disorders. The National Institute of Mental Health’s proposed Research Domain Criteria initiative incorporates a dimensional approach to assess discrete domains and constructs of behavioral function that are subserved by identifiable neural circuits. The current neurobiology of early life stress is reviewed in accordance with dimensional organization of Research Domain Criteria matrix and how the findings as a whole fit within the Research Domain Criteria frameworks.

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Gibbons, Andrew Stuart. "The neurobiology of APOE in schizophrenia and mood disorders". Frontiers in Bioscience 16, n.º 1 (2011): 962. http://dx.doi.org/10.2741/3729.

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Soares, Jair C., e Jean A. Frazier. "Neurobiology of Pediatric Mood Disorders: Are We There Yet?" Journal of Child and Adolescent Psychopharmacology 18, n.º 6 (dezembro de 2008): 549. http://dx.doi.org/10.1089/cap.2008.1865.

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Teses / dissertações sobre o assunto "Neurobiology of mood disorders"

GIORGI, MARIANI MICHELA. "MECHANISM OF ACTION OF ELECTROCONVULSIVE THERAPY (ECT): A NEUROIMMUNOCHEMICAL APPROACH". Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071492.

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Background: Electroconvulsive therapy (ECT) is one of the most effective and fast acting therapeutic options for treatment-resistant psychiatric diseases, in particular mood disorders. Mood disorders are highly heterogeneous, disabling and severe mental illness, at still unknown etiology, which have been associated with a multifaceted pathogenesis, encompassing genetic, epigenetic and metabolic vulnerabilities together psychosocial/lifestyle factors. Among the various biological patterns thought to be involved in the physiopathology of dysthymia, major depression, cyclothymia, bipolar I, II, mixed states and related disorders, alterations in the neuroendocrine and immune systems have been also evidenced. Additionally, an increasing number of studies have highlighted the relevance of impaired mechanisms of defense against reactive oxygen species (ROS) in the progression and severity of BD. Oxidative stress and redox states are indeed part of the metabolic and chemical networks of the immune/inflammation response. Despite such evidences, few studies have examined, by now, the impact of ECT on specific neuroendocrine, immune and oxidative stress paths in patients undergoing this therapy. It has been reported that ECT-induced epileptic seizures stimulate the intra-cerebral release of cytokines, including the cytokine network associated with the pathophysiology of affective disorders. It is therefore challenging to consider that the therapeutic efficacy of ECT may reside on the degree of activation of the immune/inflammatory system and that patients, under depressive, hypomanic, manic or mixed states, may change their specific profile of biochemical/immunological markers by ECT. ECT would thus act on complex biochemical cascades, formed by several neurotransmitters, neuro-hormones, neurotrophic factors and metabolic substrates, playing a significant therapeutic role. Hypothesis: Beside possible neurotransmitter and neurotrophin variations, mood disorder patients would also present significant changes of peripheral cytokine and oxidative stress profiles, before and after ECT; it might be thus possible to identify specific redox chemical and immune features related to the response/Non-response to this treatment. Such a result could also considerably help to detect peripheral molecular correlates of immunochemical dysregulation, refractory symptoms and ECT therapeutic benefits or adverse effects in mood disorders. Aims: The foremost aims of this study were: 1) to explore the degree of expression/activity of peripheral immune and oxidative stress markers during the course of ECT in bipolar patients; 2) to possibly evidence differences of these biochemical parameters among Remitter and Non-Remitter patients, assessed by means of suitable examinations and psychometric questionnaires, administered to recruited patients before, during and after ECT. Methods: From 2016 to 2018, we recruited and investigated 17 consecutive patients with a BD diagnosis accordingly to DSM-V diagnostic criteria, all treated by ECT at the Psychiatry section of the Department of Clinical and Experimental Medicine of the University of Pisa. All patients were examined during three main phases of ECT course, following this schedule: 1) at T0, by both psychometric and biochemical evaluations, before the first application; 2) at T1, by biochemical evaluations carried out 3 hours after the first application; 3) at T2, at the end of the treatment, by both psychometric and biochemical examinations. A forth biochemical assessment was carried out also at T3, 3 hours after the last application, in order to possible appraise a different reactivity of immune/oxidative stress patterns at the end of ECT applications. To constantly monitor patients, psychiatric and physical examinations were always performed for the duration of the study. Psychometric questionnaires carried out prior to (T0) and after (T3) the ECT course, consisted into: the Hamilton Depression Rating Scale-17 (HAM-D), Young Mania Rating Scale (YMRS), Brief Psychiatric Rating Scale (BPRS) and Clinical Global Improvement Impression (CGI) scale. The CGI subscale “global improvement”, final HAM-D and YMRS total scores were used to identify Remitter and Non-Remitter groups . Biochemical investigations, performed after blood samplings carried out at the 4 scheduled times, T0, T1, T2 and T3, were: 1)-the plasma levels of the immune/inflammatory cytokines IL-6, IL-8 and TNFα; 2)-the plasma levels/ activity of the antioxidant enzymes catalase (CAT) and superoxide dismutase (SOD), total thiols (R-SH), the ferric reducing ability of plasma (FRAP), uric acid as well as an index of oxidative damage, the advanced oxidation plasma protein products (AOPP). Results: At the end of therapy, about the 53% of ECT-treated BD patients was found to remit. Concerning biochemical investigation, we observed that, globally, in 17 subjects, 3 hours after ECT (T1), the activity of SOD in plasma increased nearly attaining the statistical significance, while FRAP was found significantly decreased; when analyzing Remitters and Non-Remitters separately, the nearly significant increased SOD reported in all patients at T1, after the first ECT application, was due to a greater enzyme activity in Remitters, while the global T1 FRAP reduction was due to the significant decrease of plasma ferric reducing power in Non-Remitters only. We also reported that Non-Remitters had a significantly reduced CAT activity both at T1 and in the long term, at the end of ECT course (T2), and a higher percent of responce in uric acid and IL 8 after the last ECT (T3 vs. T2). Also, Non-Remitters tended to concomitantly have, at T2, higher plasma FRAP, SOD,IL6 and lower CAT, Thiols in respect to baseline (T0) values as well as in respect to Remitters. No significant effect on the plasma level of AOPP was observed at any scheduled time in all patients, indicating that no relevant protein damage, due to ROS was reported during ECT sessions. Limitations: The study, at the present stage, had a small sample size; moreover the patient group was heterogeneous, consisting of treatment resistant bipolar patients in different phases of illness and with different pharmacological regimes. Conclusions: According to literature, we showed that ECT is an effective and safe treatment able to heal drug-resistant bipolar patients with very severe clinical presentation and risk of suicide, in all phases of the illness. Preliminary results suggest that ECT can induce changes of the antioxidant system: an increased ROS scavenging activity at T1 seems to be an index of favorable response. The diminuition of antioxidant defense system would be conversely linked to reduced benefits deriving from this therapy. The recruitment of a larger cohort of patients is needed to confirm and pursue this useful investigation of peripheral biomarkers of ECT response. This will permit to perform more robust statistical tests as multivariate regression or principal component analyses and to possibly define peculiar immunochemical changes related to the clinical response.

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Rubinsztein, Judy Sasha. "Neurocognitive processes in mood disorders". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619622.

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Maya, Vetencourt Jose' Fernando. "The antidepressant fluoxetine restores plasticity in the adult visual cortex". Doctoral thesis, Scuola Normale Superiore, 2007. http://hdl.handle.net/11384/85956.

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Chisholm, Sarah Anne. "Postnatal mood disorders : do subtypes exist?" Thesis, University of Essex, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574485.

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Background: It has been suggested that two sub types of women with postnatal depression exist. These sub types are distinguishable based on the role that childbirth plays; as either a causative or a non-specific, trigger for the depressive episode. Evidence for these proposed subtypes has been inconsistent to date. Additionally, gaps in research have also been identified relating to the existence of possible subtypes of postnatal anxiety and the differential role of childbirth in triggering anxiety during the postnatal period. Method: 98 postnatal women completed a questionnaire designed to gather information relating to symptoms of depression, general and maternal-specific dysfunctional cognitions and symptoms of state and trait anxiety. A three-step cluster analysis technique was conducted as a method of exploring the existence of subtypes within the sample recruited. Following the identification of subtypes, further statistical analysis explored the stability and validity of the cluster solutions and characteristics of the subtypes. Results: Women with postnatal depression could be categorised into subtypes based on reports of general and maternal-specific dysfunctional cognitions: a) those experiencing a depressive episode specifically related to the experience of childbirth and motherhood, and b) those experiencing a non-specific depressive episode similar to depression experienced at other time of life. Additionally, a subtype of women with postnatal depression was found who did not report any dysfunctional cognitions. Women with postnatal anxiety could be categorised into subtypes based on reports of state and trait anxiety: a) those experiencing anxiety specifically related to the experience of childbirth and motherhood, and b) those experiencing a non-specific anxious episode similar to anxiety experienced at other times of life. Implications: As well as adding to the limited amount of research exploring subtypes of postnatal mood disorders, outcomes include implications for screening and treatment of postnatal depression and anxiety.

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陸婷芝 e Ting-chi Betty Luk. "Emotion regulation and mood disorders in children". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41715366.

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Lynham, Amy. "Measuring cognition across mood and psychotic disorders". Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/116386/.

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Cognitive impairments are present in both schizophrenia and bipolar disorder and are strong predictors of functional outcomes for patients. One barrier in cognitive research of these disorders is the lack of large, well-characterised cross-disorder samples with cognitive data. The aims of this thesis were to examine cognition across the bipolar / schizophrenia diagnostic spectrum and to develop a new online cognitive battery for use in psychiatric research. Cognition was examined in participants with bipolar disorder, schizoaffective disorder and schizophrenia through a meta-analysis of existing studies and analysing data from a large well-characterised sample. The main finding was that there is a gradient of increasing cognitive impairment from bipolar disorder through schizoaffective disorder – bipolar type to schizoaffective disorder – depressive type and schizophrenia. Participants with the subtypes of schizoaffective disorder differed in their cognitive performance. Lifetime history of psychosis was associated with cognitive performance across disorders. An online cognitive battery was developed to assess the domains outlined by the Measurement and Treatment Research to Improve Cognition in Schizophrenia (MATRICS) initiative. The battery was validated against the MATRICS Consensus Cognitive Battery and showed that the tasks provided valid measurements of the majority of the MATRICS domains. A large sample of participants with a range of psychiatric disorders was recruited online. An examination of cognition in participants with major depressive disorder, bipolar disorder and schizophrenia showed that cognitive profiles were similar across disorders but participants with schizophrenia have more severe impairments than participants with bipolar disorder. An important concluding observation was that poorer cognitive performance was associated with poorer functional outcome across disorders. The findings of this thesis add to a growing literature showing the importance of examining cognitive function across psychiatric disorders. To date, it is the first study to develop and utilise an online cognitive assessment for psychiatric research.

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Luk, Ting-chi Betty. "Emotion regulation and mood disorders in children". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41715366.

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Damecour, Claire Li. "The incidence of mood disorders in aphasic patients /". Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=65395.

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Doran, Pamela. "Clinical severity and familial risk in mood disorders". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110606.

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Background: Major depressive disorder (MDD) and bipolar disorder (BP) are highly prevalent illnesses that cause substantial burden in the affected individual, their families, and society at large. These consequences underline the importance of etiological research in order to develop superior measures of both prevention and treatment. Although family history is the most consistently replicated risk factor for mood disorders, minimal efforts have been made to outline differences in sociodemographic and clinical characteristics between patients with familial and non-familial forms of these disorders. Moreover, despite the lack of conclusive findings in genome-wide association and linkage studies regarding the particular genes involved in mood disorder etiology, investigators have not yet examined the significance of familial exposure to psychiatrically ill relatives in influencing their onset and course. Methods: Subjects were 378 outpatients with a current DSM-IV diagnosis of MDD (N=139) or BP (N=239). Retrospective chart reviews were conducted in order to examine differences in sociodemographic and clinical characteristics between subjects with and without physician-reported family history. Patient-reported family history was used to compare subjects on a number of self-reported familial exposure variables. Associations between these variables and clinical characteristics were also examined. Results: Mood disorder subjects with physician-reported family history were primarily Canadian born and English speaking, and subjects without such a history were mostly unemployed. In terms of clinical characteristics, BP subjects with physician-reported family history sought psychiatric assistance at a younger age and MDD subjects without such a history were hospitalized more often. Consistent with prior research, BP subjects demonstrated more familial loading of both BP and schizophrenia/psychosis compared to MDD subjects. Furthermore, a family history of schizophrenia/psychosis and drug problems were associated with more frequent hospitalizations. Finally, a family history of drug and alcohol problems as well as living with two or more acutely ill family members, were associated with more lifetime suicide attempts. Conclusions: Family history undeniably plays an instrumental role in both the onset and clinical presentation of mood disorders. Our results particularly emphasize the significance of familial exposures and their ability to operate as risk factors, combined with underlying genetic susceptibility, to produce more severe and impairing cases of these disorders. Clinicians should carefully examine each patient's family history status since it may add value to risk assessments for outcomes like suicide attempts and hospitalizations.
Contexte: Le trouble dépressif majeur (TDM) et le trouble bipolaire (TB) sont des maladies très répandues qui causent le fardeau substantiel dans la personne touchée, leurs familles, et dans la société en général. Ces conséquences soulignent l'importance de la recherche étiologique dans le but d'élaborer des mesures supérieures à la fois de prévention et de traitement. Bien que les antécédents familiaux est le facteur de risque le plus constamment répliqué pour les troubles de l'humeur, des efforts minimes ont été apporté à décrire les différences dans les caractéristiques sociodémographiques et cliniques entre les patients avec des formes familiales et non familiales de ces troubles. Par ailleurs, malgré l'absence de résultats convaincant dans les études d'association pangénomique et les études de liaison concernant les gènes impliqués dans l'étiologie des troubles de l'humeur, les enquêteurs n'ont pas encore examiné l'importance de l'exposition aux membres de la famille souffrant d'une maladie mentale en influençant l'apparition et l'évolution des troubles de l'humeur. Méthodes: Les sujets inclus 378 patients à l'externe avec un diagnostic DSM-IV de la TDM (N=139) ou TB (N=239). Examens rétrospectifs des dossiers ont été menées afin d'examiner les différences dans les caractéristiques sociodémographiques et cliniques entre les sujets avec et sans des antécédents familiaux rapportés par un médecin. Les antécédents familiaux rapportés par le patient ont été utilisés pour comparer des sujets sur plusieurs variables auto-déclarées sur l'exposition aux membres de la famille touchée. Les associations entre ces variables et les caractéristiques cliniques ont également été examinées.Résultats: Les sujets avec un trouble de l'humeur ayant des antécédents familiaux rapportés par un médecin étaient principalement anglais et née au Canada, et les sujets sans une telle histoire étaient pour la plupart au chômage. En termes de caractéristiques cliniques, les sujets avec des antécédents familiaux de TB rapportés par un médecin a demandé l'assistance psychiatrique à un plus jeune âge et les sujets avec un TDM sans une telle histoire ont été hospitalisés plus souvent. En ligne avec la recherche précédente, les sujets avec un TB ont démontré plus de membres de la famille touchée avec soit un TB ou bien de la schizophrénie/psychose par rapport aux sujets de TDM. De plus, des antécédents familiaux de schizophrénie/psychose et de problèmes de drogue ont été associés à des hospitalisations plus fréquentes. Enfin, des antécédents familiaux de problèmes de drogue et d'alcool ainsi que de vivre avec deux ou plusieurs membres de la famille gravement malades, ont été associés à plus de tentatives de suicide à vie. Conclusions: Les antécédents familiaux jouent indéniablement un rôle instrumental dans l'apparition et à la présentation clinique des troubles de l'humeur. Nos résultats met un accent particulier sur l'importance de l'exposition aux antécédents familiaux et leur capacité à fonctionner comme facteurs de risque, en combinaison d'une sous-jacente susceptibilité génétique, pour produire des cas plus graves et débilitantes de ces troubles. Les cliniciens devraient examiner soigneusement les antécédents familiaux de chaque patient, car cela peut ajouter de la valeur aux évaluations de risque pour les tentatives de suicide et les hospitalisations.

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Taliaferro, Linda Kay. "Psychiatric Disorders as Potential Predictors in Medical Disease Development". ScholarWorks, 2011. https://scholarworks.waldenu.edu/dissertations/939.

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Millions of individuals suffer disability or death from immune-based inflammatory diseases. If psychiatric disorders could be empirically linked to the prediction of immune-based inflammatory diseases, there would be a basis for promoting disease prevention measures for individuals diagnosed with one of four psychiatric disorders. Psychoneuroimmunology provided the theoretical base for understanding emotionally induced medical disease development. In this quantitative study, a parallel archival research design was used to investigate the degree to which generalized anxiety disorder, posttraumatic stress disorder, major depression recurrent, and dysthymic disorder predicted the presence of atherosclerosis, cardiovascular heart disease, rheumatoid arthritis, cancer, and type II diabetes. There were 1,209 electronic medical records of adult patients obtained through purposive stratified sampling. A secondary data analysis was employed using descriptive cross tabulation, chi-square test of independence, and multinomial logistic regression. The findings revealed major depression recurrent was a statistically significant predictor for atherosclerosis, rheumatoid arthritis, type II diabetes and cancer. Generalized anxiety disorder was a statistically significant predictor for cancer. The results can promote positive social change by providing information that could be used to develop assessment plans that identity individuals who are at risk of developing the comorbid diseases. The prevention programs could effectively be used to minimize the subsequent development of inflammatory diseases, which in turn could decrease the onset of the medical diseases among individuals with psychiatric disorders.

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Livros sobre o assunto "Neurobiology of mood disorders"

1947-, Madden John, ed. Neurobiology of learning, emotion, and affect. New York: Raven Press, 1991.

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Neurobiology of affective disorders: The Third Annual Bristol-Myers Squibb Symposium on Neuroscience Research : October 25-26, 1991, Yale University School of Medicine. New York, N.Y: Raven Health Care Communications, 1993.

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W, Horton R., e Katona, C. L. E. 1954-, eds. Biological aspects of affective disorders. London: Academic Press, 1991.

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Power, Mick, ed. Mood Disorders. West Sussex, England: John Wiley & Sons Ltd, 2004. http://dx.doi.org/10.1002/9780470696385.

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Griez, Eric J. L., Carlo Faravelli, David J. Nutt e Joseph Zohar, eds. Mood Disorders. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470094281.

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Kocabaşoğlu, Neşe. Mood disorders. Rijeka: InTech, 2013.

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B, Keller Martin, ed. Mood disorders. Philadelphia: Saunders, 1996.

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Gold, Susan Dudley. Mood disorders. New York: Crestwood House, 1999.

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Peak, Lizabeth. Mood disorders. Detroit: Lucent Books, 2008.

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Mooney, Carla. Mood disorders. San Diego: ReferencePoint Press, 2010.

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Capítulos de livros sobre o assunto "Neurobiology of mood disorders"

Cowen, Phil J. "Neurobiology of Depression". In Mood Disorders, 189–210. Chichester, UK: John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470094281.ch7.

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Singer, Tracey, Sarah Ding e Shinghua Ding. "Astroglia Abnormalities in Post-stroke Mood Disorders". In Advances in Neurobiology, 115–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-77375-5_6.

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Lau, Jennifer Y. F. "Developmental Aspects of Mood Disorders". In Behavioral Neurobiology of Depression and Its Treatment, 15–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/7854_2012_214.

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Duman, Ronald, H. Jonathan Polan e Alan Schatzberg. "Neurobiologic Foundations of Mood Disorders". In Psychiatry, 339–53. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470515167.ch21.

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Jonathan Polan, H., Ronald Duman e Alan Schatzberg. "Neurobiologic Foundations of Mood Disorders". In Psychiatry, 341–58. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118753378.ch21.

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Gonda, Xenia, Zoltan Rihmer e Peter Dome. "Neurobiology and Pharmacological Prevention of Suicide in Mood Disorders". In Melatonin, Neuroprotective Agents and Antidepressant Therapy, 501–22. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2803-5_32.

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Tseng, Wan-Ling, Ellen Leibenluft e Melissa A. Brotman. "A Systems Neuroscience Approach to the Pathophysiology of Pediatric Mood and Anxiety Disorders". In The Neurobiology of Childhood, 297–317. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-662-45758-0_252.

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Ríos, Ulises. "A Dimensional and Dynamic Approach to the Neurobiology of Mood Disorders: On Intermediate Phenotypes and Their Interaction with Early Stress". In Depression and Personality, 167–80. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-77329-8_9.

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Harro, Jaanus. "Animal Models of Mood and Anxiety Disorders: The Pursuit of Standardization and Recognition of the Complex Neurobiology of Human Mental Health". In Neuromethods, 1–7. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2748-8_1.

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Hodes, Georgia E., e Scott J. Russo. "CHAPTER 7. The Neurobiology of Depression and Anxiety: How Do We Change from Models of Drug Efficacy to Understanding Mood and Anxiety Disorders?" In Drug Discovery, 159–83. Cambridge: Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849734943-00159.

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Trabalhos de conferências sobre o assunto "Neurobiology of mood disorders"

DOLAN, RAY J. "THE NEUROBIOLOGY OF EMOTION AND MOOD". In Proceedings of the International School of Biocybernetics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776563_0008.

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Damian, Maria-Cristina, Mihai Terpan, Doina Carina Voinescu, Alexandru Paul Baciu, Carmen Gavrila, Alexia Balta e Anamaria Ciubara. "EATING DISORDERS ASSOCIATED WITH MOOD [AFFECTIVE] DISORDERS". In The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.27.

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Introduction: Eating disorders are mental illnesses characterised by abnormal eating habits that have a negative impact on a person's physical or mental health. In the last decade hospitalizations which included eating disorders increased among all age groups. The assessment of eating disorders associated with affective disorders has important clinical implications, but the standard psychiatric classification DSM-5 (American Psychiatry Association, 2013) and ICD-10 (World Health Organization, 1993) are limited. Objectives: The current study aims to broaden the evaluation of this association and better understand its clinical implications. In addition, the study's goal is to comprehend the implications of eating disorders in Galaţi County. Method: We conducted a retrospective study on 147 patients with eating disorders and mood [affective] disorders who were admitted to the Psychiatry Hospital "Elisabeta Doamna" Galati between January 1 and February 1, 2019.We used ICD-10 (Classification of Mental and Behavioral Disorders) and DSM-5 criteria for diagnosis (Diagnostic and Statistical Manual of Mental Disorders). Results: In the period from 1 January 2019 - 1 February 2019 a total of 1131 patients was admitted in the Psychiatry Hospital, Of these, 147 were diagnosed with mood (affective) disorders, of whom 17 patients (12%) associated disorder and food as well as the independent disorder. Among these patients, the percentage of women with eating disorders associated with the affective disorder was 82 % and the percentage of men was 18 %. Conclusions: According to the findings, women are more likely to associate eating disorders with mood [affective] disorders. We also found a poor relationship between eating disorders and affective disorders, with eating disorders being associated with a high percentage of other psychiatric disorders, which is represented by alcohol and substance use, but also by high-impact diseases like Alzheimer's disease and schizophrenia.

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Nagjar, AA, M. Datta-Chaudhuri, RG Nadama e J. Robson. "Prevalence of Mood Disorders in COPD." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1464.

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Pougnet, R., e L. Pougnet. "728 Anxiety and mood disorders among junior doctors". In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.1099.

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MCMAHON, FRANCIS J. "GENETICS AND THE GLOBAL HEALTH BURDEN OF MOOD DISORDERS". In Proceedings of the International Seminar on Nuclear War and Planetary Emergencies — 27th Session. WORLD SCIENTIFIC, 2003. http://dx.doi.org/10.1142/9789812705150_0068.

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Brahem, M., M. Maraoui, H. Hachfi, S. Ben Hammouda, I. Haddada, M. Jguirim e M. Younes. "AB0346 Mood disorders (anxiety and depression) in rheumatoid arthritis". In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5279.

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de-la-Iglesia, Myriam, José-Sixto Olivar e Ruth Pinedo. "NEUROSCIENCE IN EDUCATION: AUTISM SPECTRUM DISORDER AND MOOD DISORDERS". In International Conference on Education and New Learning Technologies. IATED, 2016. http://dx.doi.org/10.21125/edulearn.2016.0454.

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Chomutare, Taridzo, Eirik Arsand e Gunnar Hartvigsen. "Mining Symptoms of Severe Mood Disorders in Large Internet Communities". In 2015 IEEE 28th International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2015. http://dx.doi.org/10.1109/cbms.2015.36.

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Hamdi, W., M. Boudokhane, I. Cherif, K. Maatallah, D. Kaffel e M. Kchir. "AB0319 Mood disorders and chronic rheumatologic diseases: about 200 cases". In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5776.

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Szabo, Christopher Paul. "MOOD DISORDERS AND SEASON OF PRESENTATION: A PRELIMINARY SOUTH AFRICAN STUDY". In IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0071.

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Relatórios de organizações sobre o assunto "Neurobiology of mood disorders"

Madu, Laura, Jacqueline Sharp e Bobby Bellflower. Efficacy of Integrating CBT for Mental Health Care into Substance Abuse Treatment in Patients with Comorbid Disorders of Substance Abuse and Mental Illness. University of Tennessee Health Science Center, abril de 2021. http://dx.doi.org/10.21007/con.dnp.2021.0004.

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Abstract: Multiple studies have found that psychiatric disorders, like mood disorders and substance use disorders, are highly comorbid among adults with either disorder. Integrated treatment refers to the treatment of two or more conditions and the use of multiple therapies such as the combination of psychotherapy and pharmacotherapy. Integrated therapy for comorbidity per numerous studies has consistently been superior to the treatment of individual disorders separately. The purpose of this QI project was to identify the effectiveness of Cognitive Behavioral Therapy (CBT) instead of current treatment as usual for treating Substance Use Disorder (SUD) or mental health diagnosis independently. It is a retrospective chart review. The review examines CBT's efficacy for engaging individuals with co-occurring mood and substance u se disorders in treatment by enhancing adherence and preventing disengagement and relapse. Methods: Forty adults aged 26-55 with a DSM-IV diagnosis of a mood disorder of Major Depressive Disorder and/or anxiety and concurrent substance use disorder (at least weekly use in the past month). Participants received 12 sessions of individual integrated CBT treatment delivered with case management over a 12-week period. Results: The intervention was associated with significant improvements in mood disorder, substance use, and coping skills at 4, 8, and 12 weeks post-treatment. Conclusions: These results provide some evidence for the effectiveness of the integrated CBT intervention in individuals with co-occurring disorders. Of note, all psychotherapies are efficacious; however, it would be more advantageous to develop a standardized CBT that identifies variables that facilitate treatment outcomes specifically to comorbid disorders of substance use and mood disorders. It is concluded that there is potentially more to be gained from further studies using randomized controlled designs to determine its efficacy.

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Haylock, Stuart. Early identification and treatment of young people at high risk of recurrent mood disorders: a feasibility study. National Institute for Health Research, agosto de 2021. http://dx.doi.org/10.3310/nihropenres.1115163.1.

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Zhou, Zhuo, Guixing Xu, Liuyang Huang, Hao Tian, Fengyuan Huang, Yilin Liu, Mingsheng Sun e Fanrong Liang. Effectiveness and Safety of Electroacupuncture for Depression: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, janeiro de 2022. http://dx.doi.org/10.37766/inplasy2022.1.0068.

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Review question / Objective: Is electroacupuncture a safe therapy for the treatment of depression? Is electroacupuncture effective for the treatment of depression, as compared with sham control, or conventional drugs？ Condition being studied: Depression is a mood disorder that causes sufferers to feel sadness, decreased interest, guilt, self-blame, loss of energy, and experience sleep disorders such as insomnia. People suffering from depression even feel they have no way out and have suicidal thoughts. In the United States, the prevalence of a major depressive disorder is 16.2%1-3. The 2010 Global Burden of Disease Study identified major depression as the second leading cause of disability worldwide and a leading cause of the burden of suicide and ischaemic heart disease. At present, depression patients are mainly treated with antidepressants, but the efficacy is extremely unstable. Studies have shown that acupuncture can help improve symptoms in patients with depression, but these clinical studies have not been systematically evaluated, and further confirmation is needed to confirm the efficacy of electroacupuncture in treating depression.

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Viswanathan, Meera, Jennifer Cook Middleton, Alison Stuebe, Nancy Berkman, Alison N. Goulding, Skyler McLaurin-Jiang, Andrea B. Dotson et al. Maternal, Fetal, and Child Outcomes of Mental Health Treatments in Women: A Systematic Review of Perinatal Pharmacologic Interventions. Agency for Healthcare Research and Quality (AHRQ), abril de 2021. http://dx.doi.org/10.23970/ahrqepccer236.

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Background. Untreated maternal mental health disorders can have devastating sequelae for the mother and child. For women who are currently or planning to become pregnant or are breastfeeding, a critical question is whether the benefits of treating psychiatric illness with pharmacologic interventions outweigh the harms for mother and child. Methods. We conducted a systematic review to assess the benefits and harms of pharmacologic interventions compared with placebo, no treatment, or other pharmacologic interventions for pregnant and postpartum women with mental health disorders. We searched four databases and other sources for evidence available from inception through June 5, 2020 and surveilled the literature through March 2, 2021; dually screened the results; and analyzed eligible studies. We included studies of pregnant, postpartum, or reproductive-age women with a new or preexisting diagnosis of a mental health disorder treated with pharmacotherapy; we excluded psychotherapy. Eligible comparators included women with the disorder but no pharmacotherapy or women who discontinued the pharmacotherapy before pregnancy. Results. A total of 164 studies (168 articles) met eligibility criteria. Brexanolone for depression onset in the third trimester or in the postpartum period probably improves depressive symptoms at 30 days (least square mean difference in the Hamilton Rating Scale for Depression, -2.6; p=0.02; N=209) when compared with placebo. Sertraline for postpartum depression may improve response (calculated relative risk [RR], 2.24; 95% confidence interval [CI], 0.95 to 5.24; N=36), remission (calculated RR, 2.51; 95% CI, 0.94 to 6.70; N=36), and depressive symptoms (p-values ranging from 0.01 to 0.05) when compared with placebo. Discontinuing use of mood stabilizers during pregnancy may increase recurrence (adjusted hazard ratio [AHR], 2.2; 95% CI, 1.2 to 4.2; N=89) and reduce time to recurrence of mood disorders (2 vs. 28 weeks, AHR, 12.1; 95% CI, 1.6 to 91; N=26) for bipolar disorder when compared with continued use. Brexanolone for depression onset in the third trimester or in the postpartum period may increase the risk of sedation or somnolence, leading to dose interruption or reduction when compared with placebo (5% vs. 0%). More than 95 percent of studies reporting on harms were observational in design and unable to fully account for confounding. These studies suggested some associations between benzodiazepine exposure before conception and ectopic pregnancy; between specific antidepressants during pregnancy and adverse maternal outcomes such as postpartum hemorrhage, preeclampsia, and spontaneous abortion, and child outcomes such as respiratory issues, low Apgar scores, persistent pulmonary hypertension of the newborn, depression in children, and autism spectrum disorder; between quetiapine or olanzapine and gestational diabetes; and between benzodiazepine and neonatal intensive care admissions. Causality cannot be inferred from these studies. We found insufficient evidence on benefits and harms from comparative effectiveness studies, with one exception: one study suggested a higher risk of overall congenital anomalies (adjusted RR [ARR], 1.85; 95% CI, 1.23 to 2.78; N=2,608) and cardiac anomalies (ARR, 2.25; 95% CI, 1.17 to 4.34; N=2,608) for lithium compared with lamotrigine during first- trimester exposure. Conclusions. Few studies have been conducted in pregnant and postpartum women on the benefits of pharmacotherapy; many studies report on harms but are of low quality. The limited evidence available is consistent with some benefit, and some studies suggested increased adverse events. However, because these studies could not rule out underlying disease severity as the cause of the association, the causal link between the exposure and adverse events is unclear. Patients and clinicians need to make an informed, collaborative decision on treatment choices.

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Which disorders precede the development of mood disorders in young people? ACAMH, dezembro de 2020. http://dx.doi.org/10.13056/acamh.14297.

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Mood disorders such as bipolar disorder (BPD) and major depressive disorder (MDD) typically emerge in childhood or adolescence. Now, researchers in Switzerland, the USA and Canada have investigated whether certain other mental health disorders precede the onset of mood disorders

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Mood Disorders and ASD: What not to miss. ACAMH, março de 2021. http://dx.doi.org/10.13056/acamh.15119.

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The autism community identified mental health as their top research priority in 2016.¹ Autistic children and adolescents are more likely than their general population counterparts to have psychiatric disorders.² For bipolar disorder, rates of 7% are seen in autistic children and adolescents versus 1% in their general population peers.

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In Conversation… Mood Disorders with Dr. Gordana Milavić. ACAMH, janeiro de 2020. http://dx.doi.org/10.13056/acamh.9940.

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Clinical characteristics of adolescents referred for treatment of depressive disorders. ACAMH, junho de 2018. http://dx.doi.org/10.13056/acamh.10557.

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Low mood and depression often emerge during adolescence and are associated with long-term difficulties including increased risk of developing other mental health disorders, educational underachievement, low income/unemployment, and risk of suicidal behaviour.

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A day in the life of a Children's Wellbeing Practitioner. ACAMH, março de 2020. http://dx.doi.org/10.13056/acamh.11564.

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Depressed mood, inattention and worry might influence the risk for other symptoms in youth. ACAMH, julho de 2020. http://dx.doi.org/10.13056/acamh.12595.

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Youth psychopathology has traditionally been conceptualized and measured at the level of disorders, which are highly heterogeneous and comorbid. However, there is growing evidence that focusing on the causes of individual symptoms might be useful.

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