Anti-P antibodies that impair memory perturb hippocampal glutamatergic receptor trafficking, synapse structure and microglia.

ABSTRACT:

Background

Anti-ribosomal P protein autoantibodies (anti-P) are associated with psychosis and cognitive dysfunction in patients with systemic lupus erythematosus (SLE), yet the underlying mechanisms remain undefined, hindering targeted therapies. Anti-P cross-react with a neuronal surface protein (NSPA), alter glutamatergic synaptic transmission and plasticity in hippocampal slices, and impair spatial memory in a short-term passive transfer mouse model. NSPA knockout mice display spatial memory deficit linked to reduced NMDAR activity and postsynaptic density (PSD) levels, along with an increased membrane-associated tyrosine phosphatase PTPMEG, suggesting disrupted glutamatergic receptor trafficking. Here, we investigated the acute effects of anti-P on receptor cell surface express

SUBMITTER: Diaz-Valdivia N 

PROVIDER: S-EPMC12465742 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature