Modulation of C5a-C5aR1 signaling alters the dynamics of AD progression.

ABSTRACT:

Background

The complement system is part of the innate immune system that clears pathogens and cellular debris. In the healthy brain, complement influences neurodevelopment and neurogenesis, synaptic pruning, clearance of neuronal blebs, recruitment of phagocytes, and protects from pathogens. However, excessive downstream complement activation that leads to generation of C5a, and C5a engagement with its receptor C5aR1, instigates a feed-forward loop of inflammation, injury, and neuronal death, making C5aR1 a potential therapeutic target for neuroinflammatory disorders. C5aR1 ablation in the Arctic (Arc) model of Alzheimer's disease protects against cognitive decline and neuronal injury without altering amyloid plaque accumulation.

Methods

To elucidate the effects of C5a-C5aR

SUBMITTER: Carvalho K 

PROVIDER: S-EPMC9277945 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature