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Titlebook: Neuroinflammatory Mechanisms in Alzheimer’s Disease; Basic and Clinical R Joseph Rogers Book 2001 Birkhäuser Verlag 2001 Alzheimer‘s diseas

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书目名称Neuroinflammatory Mechanisms in Alzheimer’s Disease
副标题Basic and Clinical R
编辑Joseph Rogers
视频video
丛书名称Progress in Inflammation Research
图书封面Titlebook: Neuroinflammatory Mechanisms in Alzheimer’s Disease; Basic and Clinical R Joseph Rogers Book 2001 Birkhäuser Verlag 2001 Alzheimer‘s diseas
描述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 th
出版日期Book 2001
关键词Alzheimer‘s disease; Alzheimer´s disease; biochemistry; chemistry; clinical research; clinical trial; cyto
版次1
doihttps://doi.org/10.1007/978-3-0348-8350-4
isbn_softcover978-3-0348-9529-3
isbn_ebook978-3-0348-8350-4Series ISSN 1422-7746 Series E-ISSN 2296-4525
issn_series 1422-7746
copyrightBirkhäuser Verlag 2001
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Cellular and molecular mechanisms of Alzheimer’s disease inflammationdiated, localized reactions in pathologically vulnerable regions of the Alzheimer’s disease (AD) brain (for previous reviews see [.-.]). The fine details of these processes are considered in subsequent chapters of this volume. Here, we summarize broadly what the mechanisms and mediators are, the evi
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Anti-inflammatory agents as possible protective factors for Alzheimer’s disease: Analysis of relevanrently available drugs may give some symptomatic relief but are not designed to prevent the disease or arrest its progression. As reviewed elsewhere in this book, many studies have now shown the presence of a chronic inflammatory reaction in affected regions of AD brain. Particularly noteworthy is t
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Role and regulation of early complement activation products in Alzheimer’s diseaseial to the onset and progression of Alzheimer’s disease (AD). How mismetabolism of APP accompanied by Aβ deposition leads to neurofibrillary changes is not completely known. A number of studies have suggested that these changes result from local inflammatory reactions ensuing in the brains of AD pat
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