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(2018) showed that acute ischemic myelin injury is initiated by vesicular release from axons, which results in cytotoxic overactivation of myelinic NMDA receptors comprising GluN2C/D subunits, which are primarily incorporated into extra-synaptic NMDA receptors (Brickley et al., We should also mention the cysteine-glutamate exchanger (xCT), which promotes glutathione synthesis by taking up cysteine and releasing glutamate, and which could possibly add to glutamate excitotoxicity evoked by ischemia and, consequently, to the overactivation of extrasynaptic NMDA receptors and neuronal death

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RNA-sequencing data analysis Samples were aligned to a combined reference genome comprising Mus musculus (mm10) and Drosophila melanogaster (release R6.35) using Rsubread (v2.2.6) (Liao et al, 2019)

Thus, their removal could be a potential therapeutic strategy which may allow the body the possibility to self-repair (92, 93)