Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 39, Issue 5-6, Pages 333-340Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0197-0186(01)00040-7
Keywords
microglial chemotaxis; amyloid beta-peptide; Alzheimer's disease
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Funding
- NIA NIH HHS [AGO7367] Funding Source: Medline
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Microglia are widely held to play important pathophysiologic roles in Alzheimer's disease (AD). On exposure to amyloid beta peptide (AP) they exhibit chemotactic. phagocytic, phenotypic and secretory responses consistent with scavenger cell activity in a localized inflammatory setting. Because AD microglial chemotaxis, phagocytosis, and secretory activity have common, tightly linked soluble intermediaries (e.g., cytokines, chemokines), cell surface intermediaries (e.g., receptors, opsonins), and stimuli (e.g., highly inert AP deposits and exposed neurofibrilly tangles), the mechanisms for microglial clearance of AP are necessarily coupled to localized inflammatory mechanisms that can be cytotoxic to nearby tissue. This presents a critical dilemma for strategies to remove AP by enhancing micoglial activation-a dilemma that warrants substantial further investigation. (C) 2001 Elsevier Science Ltd. All rights reserved.
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