The Experts below are selected from a list of 63354 Experts worldwide ranked by ideXlab platform
Wayne C Drevets - One of the best experts on this subject based on the ideXlab platform.
-
clinical application of brain imaging for the diagnosis of Mood Disorders the current state of play
Molecular Psychiatry, 2013Co-Authors: Jonathan Savitz, Wayne C Drevets, Scott L RauchAbstract:In response to queries about whether brain imaging technology has reached the point where it is useful for making a clinical diagnosis and for helping to guide treatment selection, the American Psychiatric Association (APA) has recently written a position paper on the Clinical Application of Brain Imaging in Psychiatry. The following perspective piece is based on our contribution to this APA position paper, which specifically emphasized the application of neuroimaging in Mood Disorders. We present an introductory overview of the challenges faced by researchers in developing valid and reliable biomarkers for psychiatric Disorders, followed by a synopsis of the extant neuroimaging findings in Mood Disorders, and an evidence-based review of the current research on brain imaging biomarkers in adult Mood Disorders. Although there are a number of promising results, by the standards proposed below, we argue that there are currently no brain imaging biomarkers that are clinically useful for establishing diagnosis or predicting treatment outcome in Mood Disorders.
-
neural circuits underlying the pathophysiology of Mood Disorders
Trends in Cognitive Sciences, 2012Co-Authors: Joseph L Price, Wayne C DrevetsAbstract:Although Mood Disorders constitute leading causes of disability, until recently little was known about their pathogenesis. The delineation of anatomical networks that support emotional behavior (mainly derived from animal studies) and the development of neuroimaging technologies that allow in vivo characterization of anatomy, physiology, and neurochemistry in human subjects with Mood Disorders have enabled significant advances towards elucidating the pathophysiology of major depressive disorder (MDD) and bipolar disorder (BD). In this review, we integrate insights from human and animal studies, which collectively suggest that MDD and BD involve dysfunction within an extended network including the medial prefrontal cortex and anatomically-related limbic, striatal, thalamic and basal forebrain structures.
-
Neurocircuitry of Mood Disorders
Neuropsychopharmacology, 2010Co-Authors: Joseph L Price, Wayne C DrevetsAbstract:This review begins with a brief historical overview of attempts in the first half of the 20th century to discern brain systems that underlie emotion and emotional behavior. These early studies identified the amygdala, hippocampus, and other parts of what was termed the ‘limbic’ system as central parts of the emotional brain. Detailed connectional data on this system began to be obtained in the 1970s and 1980s, as more effective neuroanatomical techniques based on axonal transport became available. In the last 15 years these methods have been applied extensively to the limbic system and prefrontal cortex of monkeys, and much more specific circuits have been defined. In particular, a system has been described that links the medial prefrontal cortex and a few related cortical areas to the amygdala, the ventral striatum and pallidum, the medial thalamus, the hypothalamus, and the periaqueductal gray and other parts of the brainstem. A large body of human data from functional and structural imaging, as well as analysis of lesions and histological material indicates that this system is centrally involved in Mood Disorders.
-
neuroimaging and neuropathological studies of depression implications for the cognitive emotional features of Mood Disorders
Current Opinion in Neurobiology, 2001Co-Authors: Wayne C DrevetsAbstract:Abstract Neuroimaging technology has provided unprecedented opportunities for elucidating the anatomical correlates of major depression. The knowledge gained from imaging research and from the postmortem studies that have been guided by imaging data is catalyzing a paradigm shift in which primary Mood Disorders are conceptualized as illnesses that involve abnormalities of brain structure, as well as of brain function. These data suggest specific hypotheses regarding the neural mechanisms underlying pathological emotional processing in Mood Disorders. They particularly support a role for dysfunction within the prefrontal cortical and striatal systems that normally modulate limbic and brainstem structures involved in mediating emotional behavior in the pathogenesis of depressive symptoms.
-
glial reduction in the subgenual prefrontal cortex in Mood Disorders
Proceedings of the National Academy of Sciences of the United States of America, 1998Co-Authors: Dost Ongur, Wayne C Drevets, Joseph L PriceAbstract:Mood Disorders are among the most common neuropsychiatric illnesses, yet little is known about their neurobiology. Recent neuroimaging studies have found that the volume of the subgenual part of Brodmann’s area 24 (sg24) is reduced in familial forms of major depressive disorder (MDD) and bipolar disorder (BD). In this histological study, we used unbiased stereological techniques to examine the cellular composition of area sg24 in two different sets of brains. There was no change in the number or size of neurons in area sg24 in Mood Disorders. In contrast, the numbers of glia were reduced markedly in both MDD and BD. The reduction in glial number was most prominent in subgroups of subjects with familial MDD (24%, P = 0.01) or BD (41%, P = 0.01). The glial reduction in subjects without a clear family history was lower in magnitude and not statistically significant. Consistent with neuroimaging findings, cortical volume was reduced in area sg24 in subjects with familial Mood Disorders. Schizophrenic brains studied as psychiatric controls had normal neuronal and glial numbers and cortical volume. Glial and neuronal numbers also were counted in area 3b of the somatosensory cortex in the same group of brains and were normal in all psychiatric groups. Glia affect several processes, including regulation of extracellular potassium, glucose storage and metabolism, and glutamate uptake, all of which are crucial for normal neuronal activity. We thus have identified a biological marker associated with familial Mood Disorders that may provide important clues regarding the pathogenesis of these common psychiatric conditions.
Eric J Nestler - One of the best experts on this subject based on the ideXlab platform.
-
the brain reward circuitry in Mood Disorders
Nature Reviews Neuroscience, 2013Co-Authors: Scott J Russo, Eric J NestlerAbstract:Recent evidence suggests that Mood Disorders are associated with altered reward function. Russo and Nestler review studies that have shown alterations in the brain reward circuitry in patients with, and animal models of, depression, and discuss the cellular and molecular underpinnings of these alterations.
-
the brain reward circuitry in Mood Disorders
Nature Reviews Neuroscience, 2013Co-Authors: Scott J Russo, Eric J NestlerAbstract:Mood Disorders are common and debilitating conditions characterized in part by profound deficits in reward-related behavioural domains. A recent literature has identified important structural and functional alterations within the brain's reward circuitry--particularly in the ventral tegmental area-nucleus accumbens pathway--that are associated with symptoms such as anhedonia and aberrant reward-associated perception and memory. This Review synthesizes recent data from human and rodent studies from which emerges a circuit-level framework for understanding reward deficits in depression. We also discuss some of the molecular and cellular underpinnings of this framework, ranging from adaptations in glutamatergic synapses and neurotrophic factors to transcriptional and epigenetic mechanisms.
Louisa G Sylvia - One of the best experts on this subject based on the ideXlab platform.
-
physical exercise for treatment of Mood Disorders a critical review
Current Behavioral Neuroscience Reports, 2016Co-Authors: Casey M Hearing, Andrew A Nierenberg, Weilynn C Chang, K L Szuhany, Thilo Deckersbach, Louisa G SylviaAbstract:The purpose of this review is to critically assess the evidence for exercise as an adjunct intervention for major depressive disorder and bipolar disorder, chronic conditions characterized by frequent comorbid conditions as well as interepisodic symptoms with poor quality of life and impaired functioning. Individuals with these Mood Disorders are at higher risk of cardiovascular disease and premature death in part because of increased rates of obesity, inactivity, and diabetes mellitus compared to the general population. Exercise may not only mitigate the increased risk of cardiovascular disease, but could also potentially improve the long term outcomes of Mood Disorders. We conducted a literature review on the impact of exercise on Mood Disorders and associated comorbid conditions as well as possible biological mechanisms. We found that exercise impacts both the physical health parameters of Mood Disorders as well as mental health outcomes. Exercise also positively impacts conditions frequently comorbid with Mood Disorders (i.e. anxiety, pain, and insomnia). There are multiple candidate biomarkers for exercise, with brain-derived neurotrophic factor and oxidative stress as two main promising components of exercise’s anti-depressant effect. Exercise appears to be a promising adjunct treatment for Mood Disorders. We conclude with recommendations for future research of exercise as an adjunct intervention for Mood Disorders.
-
physical exercise for treatment of Mood Disorders a critical review
Current Behavioral Neuroscience Reports, 2016Co-Authors: Casey M Hearing, Andrew A Nierenberg, Weilynn C Chang, K L Szuhany, Thilo Deckersbach, Louisa G SylviaAbstract:Purpose of the review The purpose of this review is to critically assess the evidence for exercise as an adjunct intervention for major depressive disorder and bipolar disorder, chronic conditions characterized by frequent comorbid conditions as well as interepisodic symptoms with poor quality of life and impaired functioning. Individuals with these Mood Disorders are at higher risk of cardiovascular disease and premature death in part because of increased rates of obesity, inactivity, and diabetes mellitus compared to the general population. Exercise may not only mitigate the increased risk of cardiovascular disease, but could also potentially improve the long term outcomes of Mood Disorders.
Scott J Russo - One of the best experts on this subject based on the ideXlab platform.
-
the brain reward circuitry in Mood Disorders
Nature Reviews Neuroscience, 2013Co-Authors: Scott J Russo, Eric J NestlerAbstract:Recent evidence suggests that Mood Disorders are associated with altered reward function. Russo and Nestler review studies that have shown alterations in the brain reward circuitry in patients with, and animal models of, depression, and discuss the cellular and molecular underpinnings of these alterations.
-
the brain reward circuitry in Mood Disorders
Nature Reviews Neuroscience, 2013Co-Authors: Scott J Russo, Eric J NestlerAbstract:Mood Disorders are common and debilitating conditions characterized in part by profound deficits in reward-related behavioural domains. A recent literature has identified important structural and functional alterations within the brain's reward circuitry--particularly in the ventral tegmental area-nucleus accumbens pathway--that are associated with symptoms such as anhedonia and aberrant reward-associated perception and memory. This Review synthesizes recent data from human and rodent studies from which emerges a circuit-level framework for understanding reward deficits in depression. We also discuss some of the molecular and cellular underpinnings of this framework, ranging from adaptations in glutamatergic synapses and neurotrophic factors to transcriptional and epigenetic mechanisms.
Roger S Mcintyre - One of the best experts on this subject based on the ideXlab platform.
-
selfish brain and selfish immune system interplay a theoretical framework for metabolic comorbidities of Mood Disorders
Neuroscience & Biobehavioral Reviews, 2017Co-Authors: Ana S Yamagata, Rodrigo B Mansur, Lucas B Rizzo, Tatiana R Rosenstock, Roger S Mcintyre, Elisa BrietzkeAbstract:Abstract According to the “selfish brain” theory, the brain regulates its own energy supply influencing the peripheral metabolism and food intake according to its needs. The immune system has been likewise “selfish” due to independent energy consumption; and it may compete with the brain (another high energy-consumer) for glucose. In Mood Disorders, stress in Mood episodes or physiological stress activate homeostasis mechanisms from the brain and the immune system to solve the imbalance. The interaction between the selfish brain and the selfish immune system may explain various conditions of medical impairment in Mood Disorders, such as Metabolic Syndrome (MetS), obesity, type 2 diabetes mellitus (T2DM) and immune dysregulation. The objective of this study is to comprehensively review the literature regarding the competition between the brain and the immune system for energy substrate. Targeting the energetic regulation of the brain and the immune system and their cross-talk open alternative treatments and a different approach in the study of general medical comorbidities in Mood Disorders, although more investigation is needed.
-
is there a metabolic Mood syndrome a review of the relationship between obesity and Mood Disorders
Neuroscience & Biobehavioral Reviews, 2015Co-Authors: Rodrigo B Mansur, Elisa Brietzke, Roger S McintyreAbstract:Obesity and Mood Disorders are highly prevalent and co-morbid. Epidemiological studies have highlighted the public health relevance of this association, insofar as both conditions and its co-occurrence are associated with a staggering illness-associated burden. Accumulating evidence indicates that obesity and Mood Disorders are intrinsically linked and share a series of clinical, neurobiological, genetic and environmental factors. The relationship of these conditions has been described as convergent and bidirectional; and some authors have attempted to describe a specific subtype of Mood Disorders characterized by a higher incidence of obesity and metabolic problems. However, the nature of this association remains poorly understood. There are significant inconsistencies in the studies evaluating metabolic and Mood Disorders; and, as a result, several questions persist about the validity and the generalizability of the findings. An important limitation in this area of research is the noteworthy phenotypic and pathophysiological heterogeneity of metabolic and Mood Disorders. Although clinically useful, categorical classifications in both conditions have limited heuristic value and its use hinders a more comprehensive understanding of the association between metabolic and Mood Disorders. A recent trend in psychiatry is to move toward a domain specific approach, wherein psychopathology constructs are agnostic to DSM-defined diagnostic categories and, instead, there is an effort to categorize domains based on pathogenic substrates, as proposed by the National Institute of Mental Health (NIMH) Research Domain Criteria Project (RDoC). Moreover, the substrates subserving psychopathology seems to be unspecific and extend into other medical illnesses that share in common brain consequences, which includes metabolic Disorders. Overall, accumulating evidence indicates that there is a consistent association of multiple abnormalities in neuropsychological constructs, as well as correspondent brain abnormalities, with broad-based metabolic dysfunction, suggesting, therefore, that the existence of a "metabolic-Mood syndrome" is possible. Nonetheless, empirical evidence is necessary to support and develop this concept. Future research should focus on dimensional constructs and employ integrative, multidisciplinary and multimodal approaches.
-
inflamed Moods a review of the interactions between inflammation and Mood Disorders
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2014Co-Authors: Joshua D Rosenblat, Rodrigo B Mansur, Danielle S Cha, Roger S McintyreAbstract:Abstract Mood Disorders have been recognized by the World Health Organization (WHO) as the leading cause of disability worldwide. Notwithstanding the established efficacy of conventional Mood agents, many treated individuals continue to remain treatment refractory and/or exhibit clinically significant residual symptoms, cognitive dysfunction, and psychosocial impairment. Therefore, a priority research and clinical agenda is to identify pathophysiological mechanisms subserving Mood Disorders to improve therapeutic efficacy. During the past decade, inflammation has been revisited as an important etiologic factor of Mood Disorders. Therefore, the purpose of this synthetic review is threefold: 1) to review the evidence for an association between inflammation and Mood Disorders, 2) to discuss potential pathophysiologic mechanisms that may explain this association and 3) to present novel therapeutic options currently being investigated that target the inflammatory–Mood pathway. Accumulating evidence implicates inflammation as a critical mediator in the pathophysiology of Mood Disorders. Indeed, elevated levels of pro-inflammatory cytokines have been repeatedly demonstrated in both major depressive disorder (MDD) and bipolar disorder (BD) patients. Further, the induction of a pro-inflammatory state in healthy or medically ill subjects induces ‘sickness behavior’ resembling depressive symptomatology. Potential mechanisms involved include, but are not limited to, direct effects of pro-inflammatory cytokines on monoamine levels, dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis, pathologic microglial cell activation, impaired neuroplasticity and structural and functional brain changes. Anti-inflammatory agents, such as acetyl-salicylic acid (ASA), celecoxib, anti-TNF-α agents, minocycline, curcumin and omega-3 fatty acids, are being investigated for use in Mood Disorders. Current evidence shows improved outcomes in Mood disorder patients when anti-inflammatory agents are used as an adjunct to conventional therapy; however, further research is needed to establish the therapeutic benefit and appropriate dosage.
-
volumetric neuroimaging investigations in Mood Disorders bipolar disorder versus major depressive disorder
Bipolar Disorders, 2008Co-Authors: Jakub Z Konarski, Roger S Mcintyre, Sidney H Kennedy, Shahryar Rafitari, Joanna K Soczynska, Terence A KetterAbstract:Background: As patients with Mood Disorders manifest heterogeneity in phenomenology, pathophysiology, etiology, and treatment response, a biological classification of mental disease is urgently needed to advance research. Patient and methodological variability complicates the comparison of neuroimaging study results and limits heuristic model development and a biologically-based diagnostic schema. Objective: We have critically reviewed and compared the magnetic resonance neuroimaging literature to determine the degree and directionality of volumetric changes in brain regions putatively implicated in the pathophysiology of major depressive disorder (MDD) versus bipolar disorder (BD). Methods: A total of 140 published magnetic resonance imaging investigations evaluating subjects with BD or MDD were selected to provide a summary and interpretation of volumetric neuroimaging results in MDD and BD. Further commentary on the pathophysiological implications, and putative cellular and pharmacological mechanisms, is also provided. Results: While whole brain volumes of patients with Mood Disorders do not differ from those of healthy controls, regional deficits in the frontal lobe, particularly in the anterior cingulate and the orbitofrontal cortex, appear to consistently differentiate subjects with Mood Disorders from the general population. Preliminary findings also suggest that subcortical structures, particularly the striatum, amygdala, and hippocampus, may be differentially affected in MDD and BD. Conclusions: Structural neuroimaging studies have consistently identified regional abnormalities in subjects with Mood Disorders. Future studies should strive to definitively establish the influence of age and medication.
