Microglial CLEC7A restrains amyloid beta plaque pathology in a mouse model of Alzheimer's disease.

ABSTRACT:

Introduction

CLEC7A is a surface receptor that is highly upregulated on microglia in many Alzheimer's disease (AD) models. Little is known about the role that microglial CLEC7A signaling plays in AD-related pathogenesis.

Methods

We utilized an inducible, central nervous system (CNS) macrophage-specific knockout of Clec7a to evaluate the role of CLEC7A in the 5xFAD mouse model of AD at 5 months of age. We used immunofluorescence microscopy, single-nuclei RNA sequencing, along with biochemical assays, to evaluate plaque burden, microglial activity, and neuronal health.

Results

CNS macrophage-targeted deletion of CLEC7A in 5xFAD mice led to a twofold increase in plaque burden, exacerbated neuritic dystrophy, and altered the expression of neuronal health genes, but did no

SUBMITTER: Mangalmurti A 

PROVIDER: S-EPMC12662145 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature