Knockout of Dectin-1 does not modify disease onset or progression in a MATR3 S85C knock-in mouse model of ALS.

ABSTRACT: Microglia have been increasingly implicated in neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). Dectin-1, encoded by the Clec7a gene, is highly upregulated in a specific microglial response state called disease-associated microglia (DAM) in various neurodegenerative conditions. However, the role of Dectin-1 in ALS is undetermined. Here, we show that Clec7a mRNA upregulation occurs in central nervous system (CNS) regions that exhibit neurodegeneration in a MATR3 S85C knock-in mouse model (Matr3 ^S85C/S85C ) of ALS. Furthermore, a significant increase in the number of Dectin-1⁺ microglia coincides with the onset of motor deficits, and this number increases with disease progression. We demonstrate that the knockout of

SUBMITTER: You J 

PROVIDER: S-EPMC11422021 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature