SOD1 and synucleinopathy: Third, our human oligodendrocyte and neuron cell culture experiments with essentially pure cells allowed the opportunity to explore directly if excitotoxic NMDA receptor activation can potentially cause synucleinopathy and oxidation/misfolding of SOD1 autonomously in these cells, thus providing proof-of-concept and new human cell models relevant to neonatal brain injury where oligodendrocytes and neurons show vulnerability [26].