Language

English

Publication Date

5-10-2022

Journal

Immunity

DOI

10.1016/j.immuni.2022.03.018

PMID

35443157

PMCID

PMC9109419

PubMedCentral® Posted Date

5-10-2023

PubMedCentral® Full Text Version

Author MSS

Abstract

The principal signals that drive memory and cognitive impairment in Alzheimer's disease (AD) remain elusive. Here, we revealed brain-wide cellular reactions to type I interferon (IFN-I), an innate immune cytokine aberrantly elicited by amyloid β plaques, and examined their role in cognition and neuropathology relevant to AD in a murine amyloidosis model. Using a fate-mapping reporter system to track cellular responses to IFN-I, we detected robust, Aβ-pathology-dependent IFN-I activation in microglia and other cell types. Long-term blockade of IFN-I receptor (IFNAR) rescued both memory and synaptic deficits and resulted in reduced microgliosis, inflammation, and neuritic pathology. Microglia-specific Ifnar1 deletion attenuated the loss of post-synaptic terminals by selective engulfment, whereas neural Ifnar1 deletion restored pre-synaptic terminals and decreased plaque accumulation. Overall, IFN-I signaling represents a critical module within the neuroinflammatory network of AD and prompts concerted cellular states that are detrimental to memory and cognition.

Keywords

Alzheimer Disease, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Animals, Disease Models, Animal, Immunity, Innate, Interferon Type I, Memory Disorders, Mice, Mice, Transgenic, Microglia, Plaque, Amyloid, interferon, memory impairment, neuroinflammation, synapse, microglia, Alzheimer’s disease

Published Open-Access

yes

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Graphical Abstract

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