Inhibition of tPA-NMDAR interaction prevents neurovascular and functional deficits induced by organophosphorus nerve agents - PubMed
10 hours ago
- #blood-brain barrier
- #therapeutic target
- #neurotoxicity
- Organophosphorus compounds (OP) like nerve agents inhibit cholinesterases, leading to excessive cholinergic signaling, excitotoxicity, and neuroinflammation.
- OP exposure increases circulating tissue-type plasminogen activator (tPA), which worsens neuroinflammation, blood-brain barrier leakage, and neurovascular coupling impairment.
- Blocking the interaction between tPA and the N-methyl-D-aspartate receptor (NMDAR) with Glunomab prevents OP-induced neurovascular and functional deficits.
- The study identifies tPA-NMDAR signaling as a key mediator of OP-induced central nervous system damage and a potential therapeutic target.