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Author: Joseph Rogers
Publisher: Birkhäuser
ISBN: 3034883501
Category : Medical
Languages : en
Pages : 266
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Book Description
Research into inflammatory mechanisms that may cause damage to the Alzheimer's disease (AD) brain has now been ongoing for nearly two decades. Some two dozen clinical studies have strongly suggested that conventional anti-inflammatory drugs may be useful to delay the onset or slow the progression of the disorder. Moreover, virtually all the major systems of the innate immune response appear to be present, and most are upregulated, in pathologically-vulnerable regions of the AD brain. These new findings are described in this volume - first in overview form, followed by chapters on topics of special interest. In many ways, to understand AD brain inflammation, one need only review a text on peripheral inflammation biology, leaving out the chapters on humoral medi ators and substituting microglia for macrophages. In several other key respects, however, AD brain inflammation is unique, due primarily to idiosyncratic interac tions of inflammatory mediators and mechanisms with classical AD pathology: amyloid ~ peptide(A~) deposits and neurofibrillary tangles (NFTs). For this reason, some key concepts about the inflammation that occurs in AD may warrant discus sion in preparation for the more detailed chapters that follow.
Author: Joseph Rogers
Publisher: Birkhäuser
ISBN: 3034883501
Category : Medical
Languages : en
Pages : 266
Get Book
Book Description
Research into inflammatory mechanisms that may cause damage to the Alzheimer's disease (AD) brain has now been ongoing for nearly two decades. Some two dozen clinical studies have strongly suggested that conventional anti-inflammatory drugs may be useful to delay the onset or slow the progression of the disorder. Moreover, virtually all the major systems of the innate immune response appear to be present, and most are upregulated, in pathologically-vulnerable regions of the AD brain. These new findings are described in this volume - first in overview form, followed by chapters on topics of special interest. In many ways, to understand AD brain inflammation, one need only review a text on peripheral inflammation biology, leaving out the chapters on humoral medi ators and substituting microglia for macrophages. In several other key respects, however, AD brain inflammation is unique, due primarily to idiosyncratic interac tions of inflammatory mediators and mechanisms with classical AD pathology: amyloid ~ peptide(A~) deposits and neurofibrillary tangles (NFTs). For this reason, some key concepts about the inflammation that occurs in AD may warrant discus sion in preparation for the more detailed chapters that follow.
Author: Joseph Rogers (Ph.D.)
Publisher: Birkhauser
ISBN: 9780817660741
Category : Alzheimer's disease
Languages : en
Pages : 261
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Book Description
Author: Gonzalo Emiliano Aranda Abreu
Publisher: BoD – Books on Demand
ISBN: 9535134515
Category : Medical
Languages : en
Pages : 320
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Book Description
"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.
Author: Paul L. Wood
Publisher: Springer Science & Business Media
ISBN: 159259297X
Category : Medical
Languages : en
Pages : 411
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Book Description
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.
Author: Morena Zusso
Publisher: Frontiers Media SA
ISBN: 2889638545
Category :
Languages : en
Pages : 282
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Book Description
Author: Arthur Liesz
Publisher: Frontiers Media SA
ISBN: 2889196917
Category : Electronic book
Languages : en
Pages : 286
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Book Description
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.
Author: National Academies of Sciences, Engineering, and Medicine
Publisher: National Academies Press
ISBN: 0309463653
Category : Medical
Languages : en
Pages : 89
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Book Description
Neuroinflammation is a burgeoning area of interest in academia and biopharma, with a broadly acknowledged role in many central nervous system (CNS) disorders. However, there is little agreement on the pathophysiological mechanisms that underlie the manifestations of neuroinflammation in the CNS compartment and how neuroinflammation operates as a driver and also as a consequence of disease in the brain. Moreover, another unclear area is how to translate increased understanding of the mechanisms that underlie neuroinflammation and its manifestations in the CNS to therapeutics. To address these gaps in understanding mechanisms and how to translate that understanding into therapeutics, the Forum on Neuroscience and Nervous System Disorders of the National Academies of Sciences, Engineering, and Medicine convened a workshop on March 20-21, 2017, bringing together key leaders in the field from industry, academia, and governmental agencies to explore the role and mechanisms of neuroinflammation in a variety of CNS diseases. The workshop also considered strategies to advance the identification and validation of biomarkers of neuroinflammation that could accelerate development of therapies, bringing much-needed treatments to patients with disorders ranging from neuroinflammatory diseases such as multiple sclerosis (MS) to neuropsychiatric disorders such as depression. This publication summarizes the presentations and discussions from the workshop.
Author: Royal Society of South Australia
Publisher:
ISBN:
Category : Science
Languages : en
Pages : 662
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Book Description
Author: Phillip K. Peterson
Publisher: Springer
ISBN: 149391071X
Category : Medical
Languages : en
Pages : 600
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Book Description
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.
Author: A.D. Roses
Publisher: Springer Science & Business Media
ISBN: 3642801099
Category : Medical
Languages : en
Pages : 208
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Book Description
There is now considerable genetic evidence that the type 4 allele of the apolipoprotein E gene is a major susceptibility factor associated with late-onset Alzheimer's disease, the common form of the disease defined as starting after sixty years of age. The role of apolipoprotein E in normal brain metabolism and in the pathogenesis of Alzheimer's disease are new and exciting avenues of research. This book, written by the most outstanding scientists in this new filed, is the first presentation of results concerning the implications of apolipoprotein E on the genetics, cell biology, neuropathology, biochemistry, and therapeutic management of Alzheimer's disease.
