The role of inflammatory processes in Alzheimer's disease

被引：72

作者：

G. Joseph Broussard

Jennifer Mytar

Rung-chi Li

Gloria J. Klapstein

机构：

[1] College of Osteopathic Medicine, Touro University California, Vallejo, CA 94592

来源：

Inflammopharmacology | 2012年 / 20卷 / 3期

关键词：

β-amyloid; Aβ; Activated endothelium; Alzheimer's disease; Amyloid; Astrocyte; Blood-brain barrier; Cardiovascular; Chemokine; Cyclooxygenase; Cytokine; Endothelial; Immune; Inflammation; Inflammatory mediators; Interleukin; Microglia; Microvessels; Neurodegenerative; Neuron; Neuronal; Pathogenesis; Pathology; Reactive nitrogen species; Reactive oxygen species; Vascular;

D O I：

10.1007/s10787-012-0130-z

中图分类号：

学科分类号：

摘要：

It has become increasingly clear that inflammatory processes play a significant role in the pathophysiology of Alzheimer's disease (AD). Neuroinflammation is characterized by the activation of astrocytes and microglia and the release of proinflammatory cytokines and chemokines. Vascular inflammation, mediated largely by the products of endothelial activation, is accompanied by the production and the release of a host of inflammatory factors which contribute to vascular, immune, and neuronal dysfunction. The complex interaction of these processes is still only imperfectly understood, yet as the mechanisms continue to be elucidated, targets for intervention are revealed. Although many of the studies to date on therapeutic or preventative strategies for AD have been narrowly focused on single target therapies, there is accumulating evidence to suggest that the most successful treatment strategy will likely incorporate a sequential, multifactorial approach, addressing direct neuronal support, general cardiovascular health, and interruption of deleterious inflammatory pathways. © 2011 CARS.

引用

页码：109 / 126

页数：17

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