Neuroinflammation And Neurodegeneration

State of the art reviews by experts in the fields of neuroscience, immunology, microbiology/infectious diseases and pharmacology addressing the convergence of the immune system (neuroinflammation) and the loss of neurons (neurodegeneration). Many of the diseases that are discussed in the book are of epidemic proportion, e.g., Alzheimer’s disease, Parkinson’s disease, stroke, viral encephalitides and substance abuse. In addition to discussions of the involvement of neuroinflammation and neurodegeneration in these disorders, scientific reviews are presented on the cells and mediators that participate in defense of and damage to the nervous system. With rare exception, no or inadequate treatment exists for the diseases discussed in this book. An underlying premise of the book is that understanding of their shared pathogenic mechanisms will lead to improved therapies. Given the rapid evolution of the field of Neuroimmune Pharmacology, readers will find this book to be the most timely and authoritative reference on the subject of each of its chapters.

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.

Recent work has implicated inflammatory processes in the pathophysiology of a variety of neurodegenerative diseases such as Alzheimer's disease, stroke and multiple sclerosis. In this book leading experts in the field discuss molecular, in vivo and clinical aspects of neuroinflammation. It is hoped, with the wealth of research being conductied in this area, that novel therapeutic targets will be identified which will allow successful therapeutic intervention in a variety of neurodegenerative diseases.

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

"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.

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.

Aging is one of the major risk factors for the onset and progression of various neurodegenerative diseases. Neuroinflammation is a common feature of virtually every central nervous system disease, and is acknowledged as a likely mediator of cognitive impairments. Systemic inflammation levels are augmented with advanced age and neurodegeneration. The influence of age on neuroinflammatory responses including glial activation, increased production of proinflammatory cytokines, and aberrant neuronal signaling could magnify the deterioration of the central nervous system microenvironment in disease, and may contribute to enhanced cognitive impairment. This eBook is a collection of highly informative original research articles, providing comprehensive aspect of neuroinflammation and possible therapeutic interventions in rescuing cognitive impairments.

The last decade has seen an upsurge of information on the role of immune responses in neurodegenerative disorders. In many of these diseases it is still unclear whether the innate and adaptive responses are pathogenic or play a role in repair, and thus understanding their precise roles is key to controlling these diseases by designing immune-therapeutic approaches. The connection between many neurological diseases is the realisation that the immune and nervous systems are inextricable linked, and that perturbations in this delicate balance are involved in many disorders. This has opened up new avenues for therapeutic approaches to treatment of CNS inflammatory and neurodegenerative disorders. Neuroinflammation and CNS Disorders brings together the very latest information on the interactions between the immune system and central nervous system. The first section of the book highlights the basic concepts in the field whilst the second section, the main body of the book, covers the role of the immune response in specific disorders of the central nervous system. Neuroinflammation and CNS Disorders will provide an invaluable guide for both researchers and clinicians working in this complex and dynamic field.