Inflammation is a central mechanism in many neurological diseases, including stroke, multiple sclerosis, and brain trauma as well as meningitis and contributes to the generation of pain. We are now beginning to understand the impact of the immune system on different nervous system functions and diseases, ranging from damage through tolerance to modulation and repair.This book discusses some of the more common neuro-inflammatory diseases. Topics covered include multiple sclerosis, optic neuritis and Susac syndrome. - Comprehensive review of the latest developments in neuroinflammation - Includes contributions from leading authorities

This book provides a comprehensive summary of the cutting edge scientific evidence regarding the role of immune system in the pathogenesis and treatment of schizophrenia and related psychotic disorders. It illustrates the role of inflammation and immunity in schizophrenia drawing on both basic science and clinical research. The chapters provide up-to-date summaries of immunological risk factors for schizophrenia and related psychotic disorders, and underlying mechanisms as informed by neuroimaging, genetic, clinical and animal experimental studies. In addition, the book will illuminate the scope for immunological treatment for schizophrenia.

Role of Inflammation in Environmental Neurotoxicity, Volume Three, in this comprehensive serial, addresses contemporary advances in neurotoxicology by providing authoritative review articles on key issues in the field. Edited by leading subject experts, topics of note in this new release include Neuroinflammation (Introduction), Organophosphates, Lead, Manganese, Drugs of abuse, Peripheral vs central inflammation, Air pollution, Developmental neurotoxicity, Ethanol, and the Blood brain barrier, amongst other topics.

"Mechanisms of Neuroinflammation" book explains how the neuronal cells become swollen at the moment of the blood-brain barrier disruption and how they lose their immunological isolation. A cascade of cytokines and immune cells from the bloodstream enters the nervous system, inflaming neurons and activating the glia. This produces a neuroinflammatory process that can generate different neurodegenerative diseases. Better understanding of mechanisms that are activated at the time when the damage to the brain occurs could lead to the development of suitable therapies that revert the neuronal inflammation and thus prevent further damage to the nervous system.

Brain edema is a simple phenomenon – an abnormal increase of brain tissue volume by the increase of brain tissue water content. However the etiology is not simple and relating to a wide variety of neurological disorders including ischemia, trauma, tumor, hemorrhage and hydrocephalus. It is still a major cause of death in the neurological/neurosurgical ward. This volume is an up-to-date report on progress in brain edema research, diagnosis and treatment, including papers presented at the 12th International Symposium on Brain Edema and Brain Tissue Injury in 2002. Major topics include molecular biology and blood-brain barrier disorders, ischemic and traumatic brain edema, imaging and diagnosis of brain edema, treatment and radiation effect. Various papers in the rapidly growing fields of neuroimaging and molecular medicine are also included.

The brain and immune system are involved in an intricate network of bidirectional communication. This relationship is vital for optimal physiological and psychological development and functioning but can also result in unwanted outcomes. In particular, this interaction plays an important role in cognition, mood and behaviour. Neuroinflammation is known to contribute to neurological and affective disorders including impaired learning and memory, depressive, anxiety and schizoaffective symptoms, as well as pain. The development of these conditions often occurs on the backdrop of pre-existing physical illnesses which give rise to increased activation of the immune system, such as cancer, obesity, infection and autoimmune disorders. Similarly, psychological states can alter regulation of the immune system. This has been most extensively studied in the context of stress and immune function. Understanding the underlying mechanisms that lead to the onset of inflammation-induced neuropathology and stress-induced immune suppression will contribute to the development of novel and effective treatment strategies for both the disease and its neurological side effects. In this research topic we explored the relationship between the immune system and the brain throughout life. We include both original research and review papers from animal, clinical and molecular perspectives.

In this thoroughly updated and revised edition of his much praised book, Paul L. Wood and a panel of leading researchers capture these new developments in a masterful synthesis of what is known today about the inflammatory mediators and cells involved in neurodegenerative diseases. This second edition contains extensive updates on the mediators produced by microglia and their role in neuroinflammatory-induced neuronal lysis. There is also increased coverage of the animal models used in the study of neuroinflammatory mechanisms, of the new imaging methods that allow the noninvasive evaluation of microglial activation in human neurodegernerative disorders, and of the role of neuroinflammation in amyloid-dependent neuronal lysis.

Type 2 Diabetes and Dementia details the relationship between diabetes, dementia and the future of medicine and therapeutics. Chapters range from epidemiology, clinical features, neuroimaging biomarkers, neuropathology, macrostructural and molecular mechanisms, risk assessment and prevention strategies, and the application of therapeutics. The book reflects the translational aspects of the current science in the field, with an emphasis on the display of neuroimaging and neuropathology. It contains contributions from world experts, and is ideal for clinicians and researchers in the fields of neurology, neuroscience, geriatric medicine and endocrinology. - Presents a comprehensive overview that details the relationship between diabetes, dementia and the future of medicine and therapeutics - Written for researchers and clinicians in neurology, neuroscience, geriatric medicine and endocrinology - Includes topics ranging from epidemiology, clinical features, neuroimaging biomarkers, neuropathology, macrostructural and molecular mechanisms, risk assessment, prevention strategies and therapeutic applications

Mechanisms of brain-immune interactions became a cutting-edge topic in systemic neurosciences over the past years. Acute lesions of the brain parenchyma, particularly, induce a profound and highly complex neuroinflammatory reaction with similar mechanistic properties between differing disease paradigms like ischemic stroke, intracerebral hemorrhage (ICH) and traumatic brain injury (TBI). Resident microglial cells sense tissue damage and initiate inflammation, activation of the endothelial brain-immune interface promotes recruitment of systemic immune cells to the brain and systemic humoral immune mediators (e.g. complements and cytokines) enter the brain through the damaged blood-brain barrier. These cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute substantially to secondary brain damage and neurodegeneration. Diverse inflammatory cascades such as pro-inflammatory cytokine secretion of invading leukocytes and direct cell-cell-contact cytotoxicity between lymphocytes and neurons have been demonstrated to mediate the inflammatory ‘collateral damage’ in models of acute brain injury. Besides mediating neuronal cell loss and degeneration, secondary inflammatory mechanisms also contribute to functional modulation of neurons and the impact of post-lesional neuroinflammation can even be detected on the behavioral level. The contribution of several specific immune cell subpopulations to the complex orchestration of secondary neuroinflammation has been revealed just recently. However, the differential vulnerability of specific neuronal cell types and the molecular mechanisms of inflammatory neurodegeneration are still elusive. Furthermore, we are only on the verge of characterizing the control of long-term recovery and neuronal plasticity after brain damage by inflammatory pathways. Yet, a more detailed but also comprehensive understanding of the multifaceted interaction of these two supersystems is of direct translational relevance. Immunotherapeutic strategies currently shift to the center of translational research in acute CNS lesion since all clinical trials investigating direct neuroprotective therapies failed. To advance our knowledge on brain-immune communications after brain damage an interdisciplinary approach covered by cellular neuroscience as well as neuroimmunology, brain imaging and behavioral sciences is crucial to thoroughly depict the intricate mechanisms.