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Specifically, recent studies in a model of ischemia/reperfusion injury in mice demonstrated that GRP78 activity was suppressed by the overexpression of p62, a macroautophagy driver (Quan et al., 2025)

Then, independent of allowing you neurons to get this easier source of energy...if the neurons are using glucose because they need energy but the glucose can't be used to repair that damage to the pentose phosphate pathway, I think that's one component of it in terms of the temporal effects, like how soon after the damage

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While the body has systems in place to repair damaged cells, persistent oxidative stress overwhelms those mechanisms, setting off a chain reaction of cellular dysfunction