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In many patients, those factors are the reason recovery feels slow in the first place

The proposed mechanism involves controlling glutamate release in the synaptic cleft, modulating NMDA receptor stimulation, affecting excitatory amino acid transporter (EAAT)-mediated reuptake, and maintaining the glutamate/glutamine cycle within astrocytes

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Researchers have investigated BPC-157 for its interactions with angiogenic signaling pathways, tissue remodeling processes, nitric oxide regulation, and cellular repair mechanisms