Microglial Phagocytosis Induced by Fibrillar β-Amyloid and IgGs Are Differentially Regulated by Proinflammatory Cytokines

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Abstract
Microglia undergo a phenotypic activation in response to fibrillar β-amyloid (fAβ) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAβ deposits. However, they can be induced to do so during Aβ vaccination therapy attributable to anti-Aβ antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Aβ plaques.