Journal articles: 'Neurobiology of mood disorders'

1

Sullivan, John L. "Neurobiology of Mood Disorders." Psychosomatics 26, no. 6 (June 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, no. 1 (January 1985): 135—a—135. http://dx.doi.org/10.1176/ajp.142.1.135-a.

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Rubin, Eugene H., and Charles F. Zorumski. "Neurobiology of Mood Disorders." Journal of Nervous and Mental Disease 173, no. 2 (February 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, no. 2 (February 1, 2002): 326—a—326. http://dx.doi.org/10.1001/archneur.59.2.326-a.

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Pande, Atul C., and Paul Max. "Book Review: Neurobiology of Mood Disorders." Canadian Journal of Psychiatry 31, no. 7 (October 1986): 693–94. http://dx.doi.org/10.1177/070674378603100721.

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Frazier, Jean A., and Jair C. Soares. "Neurobiology of Pediatric Mood Disorders: Part II." Journal of Child and Adolescent Psychopharmacology 19, no. 1 (February 2009): 1–2. http://dx.doi.org/10.1089/cap.2009.1911.

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Emery, Michael A., and 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, no. 1 (July 8, 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., and Charles B. Nemeroff. "Early Life Stress, Mood, and Anxiety Disorders." Chronic Stress 1 (February 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, no. 1 (2011): 962. http://dx.doi.org/10.2741/3729.

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Soares, Jair C., and Jean A. Frazier. "Neurobiology of Pediatric Mood Disorders: Are We There Yet?" Journal of Child and Adolescent Psychopharmacology 18, no. 6 (December 2008): 549. http://dx.doi.org/10.1089/cap.2008.1865.

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Rybakowski, Janusz K. "Recent advances in the understanding and management of bipolar disorder in adults." F1000Research 6 (November 21, 2017): 2033. http://dx.doi.org/10.12688/f1000research.12329.1.

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This article focuses on some aspects of recent progress in the neurobiology and treatment of bipolar disorder (BD) in adults. A molecular-genetic approach to the etiopathogenesis of the illness resulted in the findings of a genetic overlap between BD and other major psychiatric disorders. Furthermore, a poly-gene-environmental interaction in the development of the illness has been demonstrated. For the management of BD, new drugs with putative mood-stabilizing properties have been introduced in the past two decades. However, none of these can surpass lithium, the prototype mood-stabilizer, still considered the most specific drug for BD. Recent research on lithium, besides providing new data on the neurobiology of BD, has confirmed anti-suicidal, immunomodulatory, and neuroprotective properties of this drug.

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Gonzalez-Maeso, Javier, and J. Meana. "Heterotrimeric G Proteins: Insights into the Neurobiology of Mood Disorders." Current Neuropharmacology 4, no. 2 (April 1, 2006): 127–38. http://dx.doi.org/10.2174/157015906776359586.

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Zonana, Jessica, and Jack M. Gorman. "The Neurobiology of Postpartum Depression." CNS Spectrums 10, no. 10 (October 2005): 792–99. http://dx.doi.org/10.1017/s1092852900010312.

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AbstractPostpartum psychiatric changes can range from maternity blues to psychosis. Causality is still undetermined, but explanations for these disturbances often focus on hormonal changes and dysregulation. Researchers have begun the process of delineating what neurobiological factors may be associated with depressive disorders in pregnancy and the postpartum. This article reviews the current literature on the roles of gonadal and pituitary hormones in the psychopathophysiology of postpartum mood disorders. Other biological factors, such as biogenic amines, neuroactive steroids, cholesterol, and fatty acids, are also discussed. The potential benefits of neuroimaging to aid in understanding neuropsychiatric changes that occur in the context of postpartum depression are also considered.

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Guedes, Maiana de Oliveira, and Amanda Gilvani Cordeiro Matias. "Neuronutrition in the perspective of the prevention and treatment of depressive disorder / Neuronutrição na perspectiva da prevenção e tratamento da desordem depressiva." Brazilian Journal of Health Review 4, no. 3 (June 8, 2021): 12434–50. http://dx.doi.org/10.34119/bjhrv4n3-217.

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The father of medicine was a pioneer in suggesting the healing power of food nutrients, however it took a long time for science to recognize that food has functional properties and the ability to interfere with mood and brain health. Currently, neuroscience is showing research results, demonstrating the effectiveness of nutritional bioactive compounds with neuroprotective potential. Some metabolic changes are the basis of common neuropsychiatric diseases, such as depressive disorder, characterized by mood dysregulation, cognitive dysfunction, sleep disorders, appetite, fatigue and metabolic or inflammatory changes. Objective: to describe the potential of dietary and bioactive nutrients that interfere in the neurobiology of depressive disorder. Methodology: This is a systematic review, stratified in a time window of 2012-2021. As a search criterion for the articles, a guiding question was formulated: how does the relationship between food nutrition and its potential connections in the neurobiology of depression appear? DesCs-MESH indexes were pre-established in the English language: food nutrition, bioactive, neurobiology depressive disorders, in the vernacular: food nutrition, brain, bioactive, depressive disorder, allied to Boolean operators, to the StArt resource, to exclude duplicate manuscripts. Results: This short-review included 31 articles that met the criteria and demonstrated nutritional bioactivity involved in the neurobiological process of depressive disorder. Conclusion: the connection between diet and depression emerges with promising perspectives when demonstrating the potential of nutrients and bioactive with a neuroprotective effect. The clinical approach combined with the diet designed to produce antidepressant effects can work as an adjunct to the treatment and prevention of depressive symptoms.

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Kojima, Masami. "BDNF and mood disorders: New insights from neurobiology to applied physics." Neuroscience Research 71 (September 2011): e35-e36. http://dx.doi.org/10.1016/j.neures.2011.07.155.

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Zarate, Carlos A. "New insights into the neurobiology, diagnosis, and treatment of mood disorders." CNS Spectrums 18, no. 5 (May 22, 2013): 228–30. http://dx.doi.org/10.1017/s1092852913000254.

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Lang, Peter, Margaret Bradley, and Nicola Sambuco. "196. Neurobiology of the Anxiety and Mood Disorders: An RDoC Analysis." Biological Psychiatry 85, no. 10 (May 2019): S81. http://dx.doi.org/10.1016/j.biopsych.2019.03.210.

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18

Concerto, Carmen, Cecilia Chiarenza, Antonio Di Francesco, Antimo Natale, Ivan Privitera, Alessandro Rodolico, Antonio Trovato, et al. "Neurobiology and Applications of Inositol in Psychiatry: A Narrative Review." Current Issues in Molecular Biology 45, no. 2 (February 20, 2023): 1762–78. http://dx.doi.org/10.3390/cimb45020113.

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Inositol is a natural sugar-like compound, commonly present in many plants and foods. It is involved in several biochemical pathways, most of them controlling vital cellular mechanisms, such as cell development, signaling and nuclear processes, metabolic and endocrine modulation, cell growth, signal transduction, etc. In this narrative review, we focused on the role of inositol in human brain physiology and pathology, with the aim of providing an update on both potential applications and current limits in its use in psychiatric disorders. Overall, imaging and biomolecular studies have shown the role of inositol levels in the pathogenesis of mood disorders. However, when administered as monotherapy or in addition to conventional drugs, inositol did not seem to influence clinical outcomes in both mood and psychotic disorders. Conversely, more encouraging results have emerged for the treatment of panic disorders. We concluded that, despite its multifaceted neurobiological activities and some positive findings, to date, data on the efficacy of inositol in the treatment of psychiatric disorders are still controversial, partly due to the heterogeneity of supporting studies. Therefore, systematic use of inositol in routine clinical practice cannot be recommended yet, although further basic and translational research should be encouraged.

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19

Adler, Lenard A. "Neurobiology, Pharmacology, and Emerging Treatment." CNS Spectrums 13, S13 (2008): 4. http://dx.doi.org/10.1017/s1092852900026821.

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AbstractTreatment of attention-deficit/hyperactivity disorder (ADHD) may positively impact the neurobiology of adult patients with ADHD. Treatment may also minimize impairment from core symptoms and may alter the course of co-morbid disorders such as depression and substance use disorder. However, much of the information on stimulant use in adult ADHD comes from studies conducted in children, and it remains unclear whether there is a difference between children and adults when it comes to the side effects and tolerability of ADHD treatments. It is known that clinical presentation differs between adults and children, with adults demonstrating a higher percentage of mood disorders. Current treatments for adult ADHD include psychosocial therapies and pharmacologic therapies, the latter of which include the stimulants d-methylphenidate extended release (XR), OROS methylphenidate, lisdexamfetamine, and mixed amphetamine salts XR; and the nonstimulant atomoxetine, a selective norepinephrine reuptake inhibitor. There is need for additional study of treatment strategies for adult ADHD. Although all classes of ADHD medications are approved in adults, there are fewer approved formulations for adults than for children. Efficacy in adults is more subjective than in children, which may affect how efficacy rates for adult treatments are calculated. Adults also present a greater diversion risk than children. In addition, there are several new and emerging medication treatments worth considering.This Expert Roundtable Supplement represents part 2 of a 3-part supplement series on adult ADHD led by Lenard A. Adler, MD. In this activity, Thomas J. Spencer, MD, discusses the neurobiology and genetics of adult ADHD; Mark A. Stein, PhD, discusses stimulant therapy; and Jeffrey H. Newcorn, MD, reviews nonstimulants and psychosocial treatments.

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20

Vollenweider, Franz X., and Michael Kometer. "The neurobiology of psychedelic drugs: implications for the treatment of mood disorders." Nature Reviews Neuroscience 11, no. 9 (August 18, 2010): 642–51. http://dx.doi.org/10.1038/nrn2884.

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Fond, Guillaume, Alexandra Macgregor, Marion Leboyer, and Andreas Michalsen. "Fasting in mood disorders: neurobiology and effectiveness. A review of the literature." Psychiatry Research 209, no. 3 (October 2013): 253–58. http://dx.doi.org/10.1016/j.psychres.2012.12.018.

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22

Nascimento, M., M. Lázaro, J. Reis, G. Pereira, F. Bacelar, and A. Nobre. "Affective disorders, psychosis and lipid levels: Is there a connection? Linking psychopathology, clinical exams and neurobiology." European Psychiatry 41, S1 (April 2017): S765. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1439.

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IntroductionPublished research regarding the relationship between lipid levels in affective disorders has been contradictory. Additionally, most studies correlating psychosis to lipid serum concentrations only concern schizophrenic patients.ObjectiveTo access the relationship between serum lipid levels with the diagnosis and pathophysiology of affective disorders.MethodsDiagnostic data (ICD–10: F31–32), including mood and psychotic features, were prospectively collected for all patients admitted at the affective disorder ward at Centro Hospitalar Psiquiátrico de Lisboa (Portugal), during the third trimester of 2016. Serum concentrations of triglycerides and total/HDL/LDL cholesterol were evaluated using standard laboratory tests. Statistical analysis was performed for possible correlations between serum lipid levels and:– different stages of bipolar disorder (BD);– elevated versus depressive mood (unipolar and bipolar);– depressive mood (BD versus non-BD);– psychotic features.ResultsSixty-three patients admitted were enrolled in this study: 47 presented with BD (32 manic, 10 depressives and 5 mixed episodes) and 16 presented depressive disorders. Statistical analysis (R software) revealed that depressed bipolar patients had significantly higher triglyceride (P = 0.026), total and LDL cholesterol (P = 0.525) levels than other states; mixed episodes presented higher HDL levels (P = 0.542). Although not significant, manic patients’ HDL levels were consistently elevated compared to depressive ones, whom presented with lower values overall. Finally, when adjusted for age, psychotic patients showed lower levels of total (P = 0.031) and LDL cholesterol (P = 0.052) compared to non-psychotic patients.ConclusionsThere is a potential link between serum lipid levels and diagnosis/psychopathology of affective disorders. Further research is needed to characterize its pathophysiologic relevance.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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Brady, Roscoe, Dost Öngür, and Matcheri Keshavan. "Neurobiology of Mood-State Shifts in Bipolar Disorder." Harvard Review of Psychiatry 22, no. 1 (2014): 23–30. http://dx.doi.org/10.1097/hrp.0000000000000004.

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Cabrera, Brenda, Cristóbal Fresno, Nancy Monroy-Jaramillo, Consuelo Walss-Bass, Gabriel Fries, David Glahn, Patricia Ostrosky-Wegman, et al. "M93. BRAIN GENE EXPRESSION PROFILING OF INDIVIDUALS WITH DUAL DIAGNOSIS WHO DIED BY SUICIDE." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S170. http://dx.doi.org/10.1093/schbul/sbaa030.405.

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Abstract Background Dual diagnosis is the co-occurrence of at least one substance use disorder (SUD) and one or more mental disorders in a given individual. Despite this comorbidity is highly prevalent and associated with adverse clinical outcomes, its neurobiology remains unclear. Furthermore, patients with dual diagnosis are at higher risk for suicidal behavior in comparison with single disorder patients. Our objective was to evaluate brain gene expression patterns in individuals with dual diagnosis who died by suicide. Methods We compared the gene expression profile in the dorsolateral prefrontal cortex of suicides with DD (n= 10) to the transcriptome of suicides with SUD alone (n=10), suicides with mood disorders alone (n=13), and suicides without mental comorbidities (n=5). Gene expression profiles were assessed by microarrays. Microarray data quality control was performed. Then, microarray data were background corrected and quantile normalized. Differentially expressed genes among the conditions were identified by a linear model implemented in the limma package. Results When comparing the transcriptome of suicides with dual diagnosis to suicides with SUD alone and suicides with mood disorders alone, we identified 255 and 172 differentially expressed genes, respectively. When comparing suicides with DD to suicides without mental comorbidities, we identified 330 differentially expressed genes, mainly enriched in neurogenesis. Discussion Our results suggest that suicides with dual diagnosis present a gene expression profile distinct from that of suicides with a single disorder and suicides without mental disorders. Also, suicides with dual diagnosis, SUD and mood disorders exhibited alterations in the expression of synaptic genes. However, suicides with each condition (dual diagnosis, SUD or mood disorders) exhibited unique gene expression changes at different levels within synaptic signaling. These gene expression differences might contribute to the phenotypical and clinical discrepancies observed in patients with dual diagnosis and patients with a single disorder

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Malhi, Gin S., Pritha Das, Tim Outhred, Richard A. Bryant, Vince Calhoun, and J. John Mann. "Default mode dysfunction underpins suicidal activity in mood disorders." Psychological Medicine 50, no. 7 (May 30, 2019): 1214–23. http://dx.doi.org/10.1017/s0033291719001132.

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AbstractBackgroundSuicide is a serious and not uncommon consequence of mood disorders that occurs primarily when individuals are depressed. Understanding the neurobiology of suicidal activity (thoughts or behaviors) is likely to facilitate prevention.MethodSeventy-nine adult depressed mood disorder patients (MDP), of which 25 had attempted suicide at least once, and 66 healthy controls (HC) participated in this study. Resting-state functional MRI was used to identify neural activity differences between suicide attempters (SA) and non-attempters (NA). Specifically, differences were examined in functional connectivity both within and between four large cognitive networks [Executive Control (ECN), Default Mode (DMN), Salience (SN), and Basal Ganglia (BGN)] and their respective associations with suicidal activity.ResultsCompared to HCs, patients had greater posterior DMN activity, but less activity in the BGN, and less low-frequency spectral power in the dorso-medial DMN. Furthermore, increased posterior DMN activity in SA was associated with recent suicidal activity, whereas NA had reduced BGN activity and less dorso-medial DMN spectral power, the latter being associated with lifelong suicidal thinking. SA also had greater activity in midline circuitry compared to both HC and NA, and the pattern of BGN and DMN co-activity differed between SA and NA.ConclusionsDMN engagement raises the possibility that suicidal activity in mood disorder patients may be a consequence of impaired self-referential thought processing. Furthermore, differential BGN and DMN co-activation according to suicide attempt status suggests that attempting suicide perhaps alters cognitive flexibility. These insights are potentially useful for understanding the neural basis of suicide activity.

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Spencer, Thomas J. "Neurobiology and Genetics of ADHD in Adults." CNS Spectrums 13, S13 (2008): 5–7. http://dx.doi.org/10.1017/s1092852900026833.

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AbstractTreatment of attention-deficit/hyperactivity disorder (ADHD) may positively impact the neurobiology of adult patients with ADHD. Treatment may also minimize impairment from core symptoms and may alter the course of co-morbid disorders such as depression and substance use disorder. However, much of the information on stimulant use in adult ADHD comes from studies conducted in children, and it remains unclear whether there is a difference between children and adults when it comes to the side effects and tolerability of ADHD treatments. It is known that clinical presentation differs between adults and children, with adults demonstrating a higher percentage of mood disorders. Current treatments for adult ADHD include psychosocial therapies and pharmacologic therapies, the latter of which include the stimulants d-methylphenidate extended release (XR), OROS methylphenidate, lisdexamfetamine, and mixed amphetamine salts XR; and the nonstimulant atomoxetine, a selective norepinephrine reuptake inhibitor. There is need for additional study of treatment strategies for adult ADHD. Although all classes of ADHD medications are approved in adults, there are fewer approved formulations for adults than for children. Efficacy in adults is more subjective than in children, which may affect how efficacy rates for adult treatments are calculated. Adults also present a greater diversion risk than children. In addition, there are several new and emerging medication treatments worth considering.This Expert Roundtable Supplement represents part 2 of a 3-part supplement series on adult ADHD led by Lenard A. Adler, MD. In this activity, Thomas J. Spencer, MD, discusses the neurobiology and genetics of adult ADHD; Mark A. Stein, PhD, discusses stimulant therapy; and Jeffrey H. Newcorn, MD, reviews nonstimulants and psychosocial treatments.

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Banks, Matthew I., Zarmeen Zahid, Nathan T. Jones, Ziyad W. Sultan, and Cody J. Wenthur. "Catalysts for change: the cellular neurobiology of psychedelics." Molecular Biology of the Cell 32, no. 12 (June 1, 2021): 1135–44. http://dx.doi.org/10.1091/mbc.e20-05-0340.

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The resurgence of interest in the therapeutic potential of psychedelics for treating psychiatric disorders has rekindled efforts to elucidate their mechanism of action. In this Perspective, we focus on the ability of psychedelics to promote neural plasticity, postulated to be central to their therapeutic activity. We begin with a brief overview of the history and behavioral effects of the classical psychedelics. We then summarize our current understanding of the cellular and subcellular mechanisms underlying these drugs’ behavioral effects, their effects on neural plasticity, and the roles of stress and inflammation in the acute and long-term effects of psychedelics. The signaling pathways activated by psychedelics couple to numerous potential mechanisms for producing long-term structural changes in the brain, a complexity that has barely begun to be disentangled. This complexity is mirrored by that of the neural mechanisms underlying psychiatric disorders and the transformations of consciousness, mood, and behavior that psychedelics promote in health and disease. Thus, beyond changes in the brain, psychedelics catalyze changes in our understanding of the neural basis of psychiatric disorders, as well as consciousness and human behavior.

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Cabello-Arreola, Alejandra, Ada Man-Choi Ho, Aysegul Ozerdem, Alfredo B. Cuellar-Barboza, Mehmet U. Kucuker, Carrie J. Heppelmann, M. Cristine Charlesworth, et al. "Differential Dorsolateral Prefrontal Cortex Proteomic Profiles of Suicide Victims with Mood Disorders." Genes 11, no. 3 (February 27, 2020): 256. http://dx.doi.org/10.3390/genes11030256.

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Suicide is a major public health concern; nevertheless, its neurobiology remains unknown. An area of interest in suicide research is the dorsolateral prefrontal cortex (DLPFC). We aimed to identify altered proteins and potential biological pathways in the DLPFC of individuals who died by suicide employing mass spectrometry-based untargeted proteomics. Postmortem DLPFC from age-matched male suicide mood disorder cases (n = 5) and non-suicide mood disorder cases (n = 5) were compared. The proteins that differed between groups at false discovery rate (FDR) adjusted p-values (Benjamini–Hochberg–Yekutieli) <0.3 and Log2 fold change (FC) >|0.4| were considered statistically significant and were subjected to pathway analysis by Qiagen Ingenuity software. Thirty-three of the 5162 detected proteins showed significantly altered expression levels in the suicide cases and two of them after adjustment for body mass index. The top differentially expressed protein was potassium voltage-gated channel subfamily Q member 3 (KCNQ3) (Log2FC = −0.481, p = 2.10 × 10−09, FDR = 5.93 × 10−06), which also showed a trend to downregulation in Western blot (p = 0.045, Bonferroni adjusted p = 0.090). The most notably enriched pathway was the GABA receptor signaling pathway (p < 0.001). Here, we report a reduction trend of KCNQ3 levels in the DLPFC of male suicide victims with mood disorders. Further studies with a larger sample size and equal sex representation are needed.

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Hammack, Sayamwong E., Matthew A. Cooper, and Kimberly R. Lezak. "Overlapping neurobiology of learned helplessness and conditioned defeat: Implications for PTSD and mood disorders." Neuropharmacology 62, no. 2 (February 2012): 565–75. http://dx.doi.org/10.1016/j.neuropharm.2011.02.024.

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Grammatopoulos, Dimitris K. "Regulation of G-protein coupled receptor signalling underpinning neurobiology of mood disorders and depression." Molecular and Cellular Endocrinology 449 (July 2017): 82–89. http://dx.doi.org/10.1016/j.mce.2017.02.013.

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Rutten, Sonja, Chris Vriend, Odile A. van den Heuvel, Jan H. Smit, Henk W. Berendse, and Ysbrand D. van der Werf. "Bright Light Therapy in Parkinson's Disease: An Overview of the Background and Evidence." Parkinson's Disease 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/767105.

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Sleep disorders are common in Parkinson's disease (PD) and seem to be strongly associated with depression. It has been suggested that sleep disorders as well as depression are caused by a disturbed circadian rhythm. Indeed, PD patients are prone to misalignment of their circadian rhythm due to various factors, and many patients with PD display a phase advance of their circadian rhythm. Current treatment options for sleep disorders and depression in patients with PD are limited and can have serious side effects; alternative treatments are therefore badly needed. Bright light therapy (BLT) restores circadian rhythmicity effectively in mood- and sleep-disturbed patients without PD. The few studies that focused on the efficacy of BLT in patients with PD demonstrated a positive effect of BLT not only on sleep and mood but also on motor function. More research on the neurobiology and efficacy of BLT in PD is warranted.

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Harrison, Neil A., and Hugo D. Critchley. "Affective neuroscience and psychiatry." British Journal of Psychiatry 191, no. 3 (September 2007): 192–94. http://dx.doi.org/10.1192/bjp.bp.107.037077.

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SummaryAffective neuroscience addresses the brain mechanisms underlying emotional behaviour. In psychiatry, affective neuroscience finds application not only in understanding the neurobiology of mood disorders, but also by providing a framework for understanding the neural control of interpersonal and social behaviour and processes that underlie psychopathology. By providing a coherent conceptual framework, affective neuroscience is increasingly able to provide a mechanistic explanatory understanding of current therapies and is driving the development of novel therapeutic approaches.

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Villanueva, Rosa. "Neurobiology of Major Depressive Disorder." Neural Plasticity 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/873278.

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We survey studies which relate abnormal neurogenesis to major depressive disorder. Clinically, descriptive gene and protein expression analysis and genetic and functional studies revised here show that individual alterations of a complex signaling network, which includes the hypothalamic-pituitary-adrenal axis; the production of neurotrophins and growth factors; the expression of miRNAs; the production of proinflammatory cytokines; and, even, the abnormal delivery of gastrointestinal signaling peptides, are able to induce major mood alterations. Furthermore, all of these factors modulate neurogenesis in brain regions involved in MDD, and are functionally interconnected in such a fashion that initial alteration in one of them results in abnormalities in the others. We highlight data of potential diagnostic significance and the relevance of this information to develop new therapeutic approaches. Controversial issues, such as whether neurogenesis is the basis of the disease or whether it is a response induced by antidepressant treatments, are also discussed.

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Prossin, A. R., R. H. Yolken, M. Kamali, M. M. Heitzeg, J. B. Kaplow, W. H. Coryell, and M. G. McInnis. "Cytomegalovirus Antibody Elevation in Bipolar Disorder: Relation to Elevated Mood States." Neural Plasticity 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/939780.

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The neurobiology of mood states is complicated by exposure to everyday stressors (e.g., psychosocial, ubiquitous environmental infections like CMV), each fluctuating between latency and reactivation. CMV reactivation induces proinflammatory cytokines (e.g., TNF-α) associated with induction of neurotoxic metabolites and the presence of mood states in bipolar disorder (BD). Whether CMV reactivation is associated with bipolar diagnoses (trait) or specific mood states is unclear. We investigated 139 BD type I and 99 healthy controls to determine if concentrations of IgG antibodies to Herpesviridae (e.g., CMV, HSV-1, and HSV-2) were associated with BD-I diagnosis and specific mood states. We found higher CMV antibody concentration in BD-I than in healthy controls (T234=3.1,Puncorr=0.002;Pcorr=0.006) but no difference in HSV-1 (P>0.10) or HSV-2 (P>0.10). Compared to euthymic BD-I volunteers, CMV IgG was higher in BD-I volunteers with elevated moods (P<0.03) but not different in depressed moods (P>0.10). While relationships presented between BD-I diagnosis, mood states, and CMV antibodies are encouraging, they are limited by the study’s cross sectional nature. Nevertheless, further testing is warranted to replicate findings and determine whether reactivation of CMV infection exacerbates elevated mood states in BD-I.

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Mula, Marco, Stefano Pini, and Giovanni B. Cassano. "The neurobiology and clinical significance of depersonalization in mood and anxiety disorders: A critical reappraisal." Journal of Affective Disorders 99, no. 1-3 (April 2007): 91–99. http://dx.doi.org/10.1016/j.jad.2006.08.025.

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van Calker, Dietrich, and Knut Biber. "The Role of Glial Adenosine Receptors in Neural Resilience and the Neurobiology of Mood Disorders." Neurochemical Research 30, no. 10 (October 2005): 1205–17. http://dx.doi.org/10.1007/s11064-005-8792-1.

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Hardeland, Rüdiger. "Neurobiology, Pathophysiology, and Treatment of Melatonin Deficiency and Dysfunction." Scientific World Journal 2012 (2012): 1–18. http://dx.doi.org/10.1100/2012/640389.

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Melatonin is a highly pleiotropic signaling molecule, which is released as a hormone of the pineal gland predominantly during night. Melatonin secretion decreases during aging. Reduced melatonin levels are also observed in various diseases, such as types of dementia, some mood disorders, severe pain, cancer, and diabetes type 2. Melatonin dysfunction is frequently related to deviations in amplitudes, phasing, and coupling of circadian rhythms. Gene polymorphisms of melatonin receptors and circadian oscillator proteins bear risks for several of the diseases mentioned. A common symptom of insufficient melatonin signaling is sleep disturbances. It is necessary to distinguish between symptoms that are curable by short melatonergic actions and others that require extended actions during night. Melatonin immediate release is already effective, at moderate doses, for reducing difficulties of falling asleep or improving symptoms associated with poorly coupled circadian rhythms, including seasonal affective and bipolar disorders. For purposes of a replacement therapy based on longer-lasting melatonergic actions, melatonin prolonged release and synthetic agonists have been developed. Therapies with melatonin or synthetic melatonergic drugs have to consider that these agents do not only act on the SCN, but also on numerous organs and cells in which melatonin receptors are also expressed.

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Kato, Tadafumi. "Molecular neurobiology of bipolar disorder: a disease of ‘mood-stabilizing neurons’?" Trends in Neurosciences 31, no. 10 (October 2008): 495–503. http://dx.doi.org/10.1016/j.tins.2008.07.007.

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Katzman, Martin A., and Matthew P. Katzman. "Neurobiology of the Orexin System and Its Potential Role in the Regulation of Hedonic Tone." Brain Sciences 12, no. 2 (January 24, 2022): 150. http://dx.doi.org/10.3390/brainsci12020150.

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Orexin peptides comprise two neuropeptides, orexin A and orexin B, that bind two G-protein coupled receptors (GPCRs), orexin receptor 1 (OXR1) and orexin receptor 2 (OXR2). Although cell bodies that produce orexin peptides are localized in a small area comprising the lateral hypothalamus and adjacent regions, orexin-containing fibres project throughout the neuraxis. Although orexins were initially described as peptides that regulate feeding behaviour, research has shown that orexins are involved in diverse functions that range from the modulation of autonomic functions to higher cognitive functions, including reward-seeking, behaviour, attention, cognition, and mood. Furthermore, disruption in orexin signalling has been shown in mood disorders that are associated with low hedonic tone or anhedonia, including depression, anxiety, attention deficit hyperactivity disorder, and addiction. Notably, projections of orexin neurons overlap circuits involved in the modulation of hedonic tone. Evidence shows that orexins may potentiate hedonic behaviours by increasing the feeling of pleasure or reward to various signalling, whereas dysregulation of orexin signalling may underlie low hedonic tone or anhedonia. Further, orexin appears to play a key role in regulating behaviours in motivationally charged situations, such as food-seeking during hunger, or drug-seeking during withdrawal. Therefore, it would be expected that dysregulation of orexin expression or signalling is associated with changes in hedonic tone. Further studies investigating this association are warranted.

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Stein, Mark A. "Treating Adult ADHD with Stimulants." CNS Spectrums 13, S13 (2008): 8–11. http://dx.doi.org/10.1017/s1092852900026845.

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AbstractTreatment of attention-deficit/hyperactivity disorder (ADHD) may positively impact the neurobiology of adult patients with ADHD. Treatment may also minimize impairment from core symptoms and may alter the course of co-morbid disorders such as depression and substance use disorder. However, much of the information on stimulant use in adult ADHD comes from studies conducted in children, and it remains unclear whether there is a difference between children and adults when it comes to the side effects and tolerability of ADHD treatments. It is known that clinical presentation differs between adults and children, with adults demonstrating a higher percentage of mood disorders. Current treatments for adult ADHD include psychosocial therapies and pharmacologic therapies, the latter of which include the stimulants d-methylphenidate extended release (XR), OROS methylphenidate, lisdexamfetamine, and mixed amphetamine salts XR; and the nonstimulant atomoxetine, a selective norepinephrine reuptake inhibitor. There is need for additional study of treatment strategies for adult ADHD. Although all classes of ADHD medications are approved in adults, there are fewer approved formulations for adults than for children. Efficacy in adults is more subjective than in children, which may affect how efficacy rates for adult treatments are calculated. Adults also present a greater diversion risk than children. In addition, there are several new and emerging medication treatments worth considering.This Expert Roundtable Supplement represents part 2 of a 3-part supplement series on adult ADHD led by Lenard A. Adler, MD. In this activity, Thomas J. Spencer, MD, discusses the neurobiology and genetics of adult ADHD; Mark A. Stein, PhD, discusses stimulant therapy; and Jeffrey H. Newcorn, MD, reviews nonstimulants and psychosocial treatments.

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Newcorn, Jeffrey H. "Nonstimulants and Emerging Treatments in Adults with ADHD." CNS Spectrums 13, S13 (2008): 12–16. http://dx.doi.org/10.1017/s1092852900026857.

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AbstractTreatment of attention-deficit/hyperactivity disorder (ADHD) may positively impact the neurobiology of adult patients with ADHD. Treatment may also minimize impairment from core symptoms and may alter the course of co-morbid disorders such as depression and substance use disorder. However, much of the information on stimulant use in adult ADHD comes from studies conducted in children, and it remains unclear whether there is a difference between children and adults when it comes to the side effects and tolerability of ADHD treatments. It is known that clinical presentation differs between adults and children, with adults demonstrating a higher percentage of mood disorders. Current treatments for adult ADHD include psychosocial therapies and pharmacologic therapies, the latter of which include the stimulants d-methylphenidate extended release (XR), OROS methylphenidate, lisdexamfetamine, and mixed amphetamine salts XR; and the nonstimulant atomoxetine, a selective norepinephrine reuptake inhibitor. There is need for additional study of treatment strategies for adult ADHD. Although all classes of ADHD medications are approved in adults, there are fewer approved formulations for adults than for children. Efficacy in adults is more subjective than in children, which may affect how efficacy rates for adult treatments are calculated. Adults also present a greater diversion risk than children. In addition, there are several new and emerging medication treatments worth considering.This Expert Roundtable Supplement represents part 2 of a 3-part supplement series on adult ADHD led by Lenard A. Adler, MD. In this activity, Thomas J. Spencer, MD, discusses the neurobiology and genetics of adult ADHD; Mark A. Stein, PhD, discusses stimulant therapy; and Jeffrey H. Newcorn, MD, reviews nonstimulants and psychosocial treatments

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Heim, Christine, and Charles B. Nemeroff. "The role of childhood trauma in the neurobiology of mood and anxiety disorders: preclinical and clinical studies." Biological Psychiatry 49, no. 12 (June 2001): 1023–39. http://dx.doi.org/10.1016/s0006-3223(01)01157-x.

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Trzesniak, C., M. S. Schaufelberger, F. L. S. Duran, L. C. Santos, P. G. P. Rosa, P. K. McGuire, R. M. Murray, et al. "Longitudinal follow-up of cavum septum pellucidum and adhesio interthalamica alterations in first-episode psychosis: a population-based MRI study." Psychological Medicine 42, no. 12 (April 27, 2012): 2523–34. http://dx.doi.org/10.1017/s0033291712000839.

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BackgroundNeurodevelopmental alterations have been described inconsistently in psychosis probably because of lack of standardization among studies. The aim of this study was to conduct the first longitudinal and population-based magnetic resonance imaging (MRI) evaluation of the presence and size of the cavum septum pellucidum (CSP) and adhesio interthalamica (AI) in a large sample of patients with first-episode psychosis (FEP).MethodFEP patients (n=122) were subdivided into schizophrenia (n=62), mood disorders (n=46) and other psychosis (n=14) groups and compared to 94 healthy next-door neighbour controls. After 13 months, 80 FEP patients and 52 controls underwent a second MRI examination.ResultsWe found significant reductions in the AI length in schizophrenia FEP in comparison with the mood disorders and control subgroups (longer length) at the baseline assessment, and no differences in any measure of the CSP. By contrast, there was a diagnosis×time interaction for the CSP length, with a more prominent increase for this measure in the psychosis group. There was an involution of the AI length over time for all groups but no diagnosis×time interaction.ConclusionsOur findings suggest that the CSP per se may not be linked to the neurobiology of emerging psychotic disorders, although it might be related to the progression of the disease. However, the fact that the AI length was shown to be shorter at the onset of the disorder supports the neurodevelopmental model of schizophrenia and indicates that an alteration in this grey matter junction may be a risk factor for developing psychosis.

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Hoppes, Kimberly. "The Application of Mindfulness-Based Cognitive Interventions in the Treatment of Co-occurring Addictive and Mood Disorders." CNS Spectrums 11, no. 11 (November 2006): 829–51. http://dx.doi.org/10.1017/s1092852900014991.

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ABSTRACTThis article reviews the theory, clinical application, and empirical findings on mindfulness–based cognitive therapy (MBCT) for mental health and addictive disorders. Expanding upon the research demonstrating the efficacy of cognitive-behavioral therapy (CBT) for addiction, this article develops and explores the rationale for combining mindfulness-based interventions with evidence-based CBTs in treating addictive disorders, with an emphasis on substance use disorders with co-occurring mood disorders.This article proposes that deficits in affect regulation — related to the behavioral and emotional effects of neurobiological changes that occur with longterm substance abuse — pose a unique set of challenges in early recovery. Prolonged use of addictive substances impairs the brain pathways to detach or maintain perspective in response to strong emotional states. In treating this affective dysregulation, which can contribute to the vulnerability to relapse in the early stages of recovery, the affect–regulation-specific focus of MBCT adds a valuable element to augment CBT for addiction. Summarizing magnetic resonance imaging and positron emission tomography findings on the effects of MBCT and the neurobiology of drug addiction, this article out-lines directions for further research on potential benefits of MBCT for the recovering individual. Finally, this article describes a structured protocol, developed at the Mount Sinai School of Medicine in New York City, which combines CBT with mindfulness-based intervention, for the treatment of affect-regulation issues specific to co-occurring addictive and mood disorders.

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Cunha E Costa, N., S. Cruz, and G. Sobreira. "Overlap between substance and behavioural addictions: substance abuse in patients with pathological gambling." European Psychiatry 65, S1 (June 2022): S832. http://dx.doi.org/10.1192/j.eurpsy.2022.2155.

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Introduction Pathological gambling consists of a persistent and maladaptive pattern of gambling behavior, that often leads to significant adverse psychosocial and financial outcomes. It is currently classified as an “Impulse Disorder” on ICD-10 but the DSM-5 moved this diagnosis from “Impulse-Control Disorders” to “Substance-Related and Addictive Disorders” section[1]. Behavioral addictions, especially pathological gambling, share many features with substance dependences, namely clinical findings and behavioural patterns, comorbidity with psychiatric disorders, genetic factors and family history, neurobiology, natural history and response to treatment[2]. Objectives To study the impact of substance abuse in patients with pathological gambling. Methods Literary review, using PubMed database search, regarding substance abuse and pathological gambling. Results 57,5% of individuals with pathological gambling also present with some form of substance use[3].There was also a large percentage of patients presenting with nicotine dependence (60,1%) and a fourfold increase in the risk of developing an alcohol use disorder[3]. Individuals with substance use disorders also show a threefold risk of developing pathological gambling and substance use appears to negatively influence gambling behaviours in this population. Gambling habits in adolescents have been linked to an increased risk of current and lifetime drug use of multiple substances[4]. Other psychiatric comorbidities were also frequent in this population: 37.9% of patients presented with mood disorders and 37.4% with anxiety disorders[3]. Conclusions There is a significant clinical and neurobiological overlap between substance use disorders and pathological gambling. Individuals with pathological gambling have a high prevalence of substance use disorders and an increased lifetime risk of substance use, which negatively influences gambling behavior. Disclosure No significant relationships.

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Lenzi, Alessandro, Fabrizio Lazzerini, and Donatella Marazziti. "The Current Course of Mood Disorders: A 3-Year Follow-Up." CNS Spectrums 4, no. 5 (May 1999): 77–82. http://dx.doi.org/10.1017/s1092852900011755.

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AbstractThe aim of this study was to evaluate the natural course of mood disorders in 157 patients admitted consecutively to the Dipartimento di Psichiatria, Neurobiologia, Farmacologia e Biotecnologie at Pisa University for an affective or schizoaffective episode and followed for 3 years.During the follow-up, three patients committed suicide and three died of natural causes. The three suicide patients were diagnosed as suffering from a depressive episode deriving from Bipolar I disorder. Of the remaining 104 patients, 42% had no relapses, 35% had up to three relapses, and 23% had more than three relapses; there were no significant differences between these three groups.In conclusion, recent treatments seem able to reduce the length and number of relapses in patients with mood disorders. The hyperthymic temperament seems to be a characteristic of compliant patients and a predictor of a good response to treatment. The mortality rate connected with somatic or accidental causes appears to be similar to that of the general population, while the rate of suicide is higher.

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Liebowitz, Michael R., David L. Ginsberg, Philip T. Ninan, Franklin R. Schneier, and Carlos Blanco. "Integrating Neurobiology and Psychopathology into Evidence-Based Treatment of Social Anxiety Disorder." CNS Spectrums 10, no. 10 (October 2005): 805a—805b. http://dx.doi.org/10.1017/s1092852900010336.

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AbstractSocial anxiety disorder (SAD) is a common, chronic psychiatric disorder characterized by a persistent fear of social or performance situations in which embarrassment can occur. This disorder typically appears during the mid-adolescent years and is unremitting throughout life if not properly treated. SAD presents as two subtypes: the more common and debilitating generalized form, and the nongeneralized form, which consists predominantly of performance anxiety. The majority of patients with SAD have comorbid mental disorders, including mood, anxiety, and substance abuse. No single development theory has been proposed to account for the origins of SAD, although current understanding of the etiology of SAD posits an interaction between psychological and biological factors. Risk factors include environmental and parenting influences and dysfunctional cognitive and conditioning events in early childhood. The neurobiology of SAD appears to involve neurochemical dysfunction, as evidenced by studies of neuroreceptor imaging, neuroendocrine function, and profiles of response to specific medications. Clinical trials have demonstrated that benzodiazepines and antidepressants are effective in the treatment of SAD. The selective serotonin reuptake inhibitors are emerging as the first-line treatment for SAD, based on their proven safety, tolerability, and efficacy. Goals for ongoing future research include development of approaches to achieve remission, to convert nonresponders and partial responders to full responders, and to prevent relapse and maintain long-term efficacy.This monograph explores the epidemiology, clinical presentation, and differential diagnosis of SAD, with a focus on neural circuitry of social relationships and neurochemical dysfunction. The prevalence, rates of recognition and treatment, patterns of comorbidity, quality-of-life issues, and natural history of SAD are discussed as well as pharmacologic and psychosocial treatment strategies for SAD.

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Liebowitz, Michael R., Philip T. Ninan, Franklin R. Schneier, Carlos Blanco, David L. Ginsberg, and Eric Hollander. "Integrating Neurobiology and Psychopathology into Evidence-Based Treatment of Social Anxiety Disorder." CNS Spectrums 10, S13 (September 2005): 1–2. http://dx.doi.org/10.1017/s1092852900028066.

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AbstractSocial anxiety disorder (SAD) is a common, chronic psychiatric disorder characterized by a persistent fear of social or performance situations in which embarrassment can occur. This disorder typically appears during the mid-adolescent years and is unremitting throughout life if not properly treated. SAD presents as two subtypes: the more common and debilitating generalized form, and the nongeneralized form, which consists predominantly of performance anxiety. The majority of patients with SAD have comorbid mental disorders, including mood, anxiety, and substance abuse. No single development theory has been proposed to account for the origins of SAD, although current understanding of the etiology of SAD posits an interaction between psychological and biological factors. Risk factors include environmental and parenting influences and dysfunctional cognitive and conditioning events in early childhood. The neurobiology of SAD appears to involve neurochemical dysfunction, as evidenced by studies of neuroreceptor imaging, neuroendocrine function, and profiles of response to specific medications. Clinical trials have demonstrated that benzodiazepines and antidepressants are effective in the treatment of SAD. The selective serotonin reuptake inhibitors are emerging as the first-line treatment for SAD, based on their proven safety, tolerability, and efficacy. Goals for ongoing future research include development of approaches to achieve remission, to convert nonresponders and partial responders to full responders, and to prevent relapse and maintain long-term efficacy.This monograph explores the epidemiology, clinical presentation, and differential diagnosis of SAD, with a focus on neural circuitry of social relationships and neurochemical dysfunction. The prevalence, rates of recognition and treatment, patterns of comorbidity, quality-of-life issues, and natural history of SAD are discussed as well as pharmacologic and psychosocial treatment strategies for SAD.

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Robinson, Emma S. J. "Translational new approaches for investigating mood disorders in rodents and what they may reveal about the underlying neurobiology of major depressive disorder." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1742 (January 29, 2018): 20170036. http://dx.doi.org/10.1098/rstb.2017.0036.

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Mood disorders represent one of society's most costly and challenging health burdens. The drug treatments used today were initially discovered serendipitously in the 1950s. Animal models were then developed based on the ability of these drugs to alter specific behaviours. These models have played a major role in the development of the second generation of antidepressants. However, their use has been heavily criticized, particularly in relation to whether they recapitulate similar underlying biology to the psychiatric disorder they are proposed to represent. This article considers our work in the field of affective bias and the development of a translational research programme to try to develop and validate better animal models. We discuss whether the new data that have arisen from these studies support an alternative perspective on the underlying neurobiological processes that lead to major depressive disorder (MDD). Specifically, this article will consider whether a neuropsychological mechanism involving affective biases plays a causal role in the development of MDD and its associated emotional and behavioural symptoms. These animal studies also raise the possibility that neuropsychological mechanisms involving affective biases are a precursor to, rather than a consequence of, the neurotrophic changes linked to MDD. This article is part of a discussion meeting issue ‘Of mice and mental health: facilitating dialogue between basic and clinical neuroscientists’.

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Albert, Paul R., Chawki Benkelfat, and Laurent Descarries. "The neurobiology of depression—revisiting the serotonin hypothesis. I. Cellular and molecular mechanisms." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1601 (September 5, 2012): 2378–81. http://dx.doi.org/10.1098/rstb.2012.0190.

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The serotonin (5-HT) hypothesis of depression dates from the 1960s. It originally postulated that a deficit in brain serotonin, corrected by antidepressant drugs, was the origin of the illness. Nowadays, it is generally accepted that recurring mood disorders are brain diseases resulting from the combination, to various degrees, of genetic and other biological as well as environmental factors, evolving through the lifespan. All areas of neuroscience, from genes to behaviour, molecules to mind, and experimental to clinical, are actively engaged in attempts at elucidating the pathophysiology of depression and the mechanisms underlying the efficacy of antidepressant treatments. This first of two special issues of Philosophical Transactions B seeks to provide an overview of current developments in the field, with an emphasis on cellular and molecular mechanisms, and how their unravelling opens new perspectives for future research.

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Journal articles on the topic 'Neurobiology of mood disorders'

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