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Remarkably PIRA-like disability accumulation was also observed in pediatric MS raising the possibility that an underlying degenerative process can start very early (De Stefano et al., 2010

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