Specifically, neuronal TNFR1 and IKKβ both advance the onset of inflammatory demyelination, neuronal TNFR1 is further required for axon damage and oligodendrocyte (OLG) loss during cuprizone-induced (CPZ) demyelination, and neuronal TNFR2 increases protection against glutamate excitotoxicity in vitro and in vivo. Here, TNFRSF1A is linked to Peripheral demyelination.