Mice deficient in complement C3 are protected against recognition memory deficits and astrogliosis induced by status epilepticus.

ABSTRACT:

Introduction

Status epilepticus (SE) can significantly increase the risk of temporal lobe epilepsy (TLE) and cognitive comorbidities. A potential candidate mechanism underlying memory defects in epilepsy may be the immune complement system. The complement cascade, part of the innate immune system, modulates inflammatory and phagocytosis signaling, and has been shown to contribute to learning and memory dysfunctions in neurodegenerative disorders. We previously reported that complement C3 is elevated in brain biopsies from human drug-resistant epilepsy and in experimental rodent models. We also found that SE-induced increases in hippocampal C3 levels paralleled the development of hippocampal-dependent spatial learning and memory deficits in rats. Thus, we hypothesized that SE-induce

SUBMITTER: Schartz ND 

PROVIDER: S-EPMC10682718 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature