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Major depression is a highly prevalent disorder that poses a significant social burden in society nowadays. The pathophysiology of this disease is still poorly understood but growing evidence suggests that impaired neuron and glial plasticity may be a key underlying mechanism for the precipitation of the disorder. One of the most surprising findings in this field was the involvement of glial cells in the pathophysiology of major depression and in the action of antidepressants, namely in mechanisms related with adult neurogenesis imbalances or dendritic arborization impairments. In particular, several works refer to alterations in the morphology and numbers of astrocytes, microglia and oligodendrocytes in the context of depression in human patients or animal models of depression. These observations were linked to functional evidences and suggested to underlie the pathophysiology of depression. Among others, these include impairments in the cross-talk between glia and neurons, changes in the level of neurotransmitter or immunoactive substances, myelination status, synapse formation, maintenance, or elimination. In addition to the implication of glia in the pathophysiology of depression, a number of studies is ascribing glia pathways to classically accepted antidepressant mechanisms. Therefore, it is noteworthy to elucidate the role of glia in the effect provided by antidepressant treatment in order to better understand secondary effects and elucidate alternative targets for treatment.
Major depression is a highly prevalent disorder that poses a significant social burden in society nowadays. The pathophysiology of this disease is still poorly understood but growing evidence suggests that impaired neuron and glial plasticity may be a key underlying mechanism for the precipitation of the disorder. One of the most surprising findings in this field was the involvement of glial cells in the pathophysiology of major depression and in the action of antidepressants, namely in mechanisms related with adult neurogenesis imbalances or dendritic arborization impairments. In particular, several works refer to alterations in the morphology and numbers of astrocytes, microglia and oligodendrocytes in the context of depression in human patients or animal models of depression. These observations were linked to functional evidences and suggested to underlie the pathophysiology of depression. Among others, these include impairments in the cross-talk between glia and neurons, changes in the level of neurotransmitter or immunoactive substances, myelination status, synapse formation, maintenance, or elimination. In addition to the implication of glia in the pathophysiology of depression, a number of studies is ascribing glia pathways to classically accepted antidepressant mechanisms. Therefore, it is noteworthy to elucidate the role of glia in the effect provided by antidepressant treatment in order to better understand secondary effects and elucidate alternative targets for treatment.
First Published in 1995. Routledge is an imprint of Taylor & Francis, an informa company.
Recent studies regarding the neuropathology of specific neurological disorders suggest that both neurodevelopmental and neurodegenerative processes may play a role. However, in contrast to the neurodegeneration seen in neurological disorders such as Parkinson's and Alzheimer's disease, the term "neuroprogression" has been used to describe the neurodevelopmental aspect of pathological brain re-wiring that takes place in the context of severe psychiatric disorders, such as schizophrenia or bipolar disorder. Within psychiatry, patients with severe psychopathology, such as those depressed patients who eventually commit suicide, have been shown to present with increased inflammatory markers in the brain. A similar increase in inflammatory markers is also found in patients with bipolar disorders and schizophrenia. Thus, oxidative stress, inflammation, and changes in growth factors are thought to be the pathways of neuroprogression. Neuroprogression in Psychiatry provides a comprehensive summary of the current developments in the emerging field of neuroprogression. With contributions by leading researchers in the field, this book examines the role of neuroprogression across a wide range of specific psychiatric disorders, with chapters included on major depressive disorder, anxiety disorder, post-traumatic stress disorder, substance abuse, schizophrenia, and bipolar disorder.
This book reviews all aspects of major depressive disorder (MDD), casting light on its neurobiological underpinnings and describing the most recent advances in management. The book is divided into four sections, the first of which discusses MDD from a network science perspective, highlighting the alterations in functional and structural connectivity and presenting insights achieved through resting state functional MRI and the development of neuroimaging-based biomarkers. The second section examines important diagnostic and neurobiological issues, while the third considers the currently available specific treatments for MDD, including biofeedback, neurofeedback, cognitive behavioral therapy, acceptance and commitment therapy, neuromodulation therapy, psychodynamic therapy, and complementary and alternative medicine. A concluding section is devoted to promising emerging treatments, from novel psychopharmacological therapies through to virtual reality treatment, immunotherapy, biomarker-guided tailored therapy, and more. Written by leading experts from across the world, the book will be an excellent source of information for both researchers and practitioners.
With recent studies using genetic, epigenetic, and other molecular and neurochemical approaches, a new era has begun in understanding pathophysiology of suicide. Emerging evidence suggests that neurobiological factors are not only critical in providing potential risk factors but also provide a promising approach to develop more effective treatment and prevention strategies. The Neurobiological Basis of Suicide discusses the most recent findings in suicide neurobiology. Psychological, psychosocial, and cultural factors are important in determining the risk factors for suicide; however, they offer weak prediction and can be of little clinical use. Interestingly, cognitive characteristics are different among depressed suicidal and depressed nonsuicidal subjects, and could be involved in the development of suicidal behavior. The characterization of the neurobiological basis of suicide is in delineating the risk factors associated with suicide. The Neurobiological Basis of Suicide focuses on how and why these neurobiological factors are crucial in the pathogenic mechanisms of suicidal behavior and how these findings can be transformed into potential therapeutic applications.
A practical guide on how to assess and treat schizophrenia and related disorders using cognitive rehabilitation.
Traditionally, abnormalities of neurons and neuronal networks including synaptic abnormalities and disturbance of neurotransmitters have dominantly been believed to be the main causes of psychiatric disorders. Recent cellular neuroscience has revealed various unknown roles of glial cells such as astrocytes, oligodendrocytes and microglia. These glial cells have proved to continuously contact with neurons /synapses, and have been shown to play important roles in brain development, homeostasis and various brain functions. Beyond the classic neuronal doctrine, accumulating evidence has suggested that abnormalities and disturbances of neuron-glia crosstalk may induce psychiatric disorders, while these mechanisms have not been well understood. This Research Topic of the Frontiers in Cellular Neuroscience will focus on the most recent developments and ideas in the study of glial cells (astrocytes, oligodendrocytes and microglia) focusing on psychiatric disorders such as schizophrenia, mood disorders and autism. Not only molecular, cellular and pharmacological approaches using in vitro / in vivo experimental methods but also translational research approaches are welcome. Novel translational research approaches, for example, using novel techniques such as induced pluripotent stem (iPS) cells, may lead to novel solutions. We believe that investigations to clarify the correlation between glial cells and psychiatric disorders contribute to a novel understanding of the pathophysiology of these disorders and the development of effective treatment strategies.
The Advances in Pharmacology series presents a variety of chapters from the best authors in the field. - Includes the authority and expertise of leading contributors in pharmacology - Presents the latest release in the Advances in Pharmacology series