Circulating immune cells contribute to the pathogenesis of Alzheimer’s disease (AD), but their role is poorly understood. Rosenzweig et al. recently identified a subset of interleukin (IL)-17+ neutrophils that inhibit neuroprotective microglia in female APOE4 carriers. Blockade of IL-17 signaling or APOE4 deletion in neutrophils restored microglial responses and reduced murine amyloid pathology.
APOE4 affects neutrophil-microglia crosstalk in Alzheimer's disease
Terrabuio EWriting – Original Draft Preparation
;Constantin G
2024-01-01
Abstract
Circulating immune cells contribute to the pathogenesis of Alzheimer’s disease (AD), but their role is poorly understood. Rosenzweig et al. recently identified a subset of interleukin (IL)-17+ neutrophils that inhibit neuroprotective microglia in female APOE4 carriers. Blockade of IL-17 signaling or APOE4 deletion in neutrophils restored microglial responses and reduced murine amyloid pathology.
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