SOD1 and Cerebral ischemia: Perhaps more relevant, a murine model expressing a modest 50 % reduction in SOD1 protein (Sod1+/−) elicits modest motor dysfunction and increases neuronal susceptibility to degeneration following axotomy[174] and other cellular stressors such as glutamate toxicity,[175] cerebral ischemia,[176] and aging.[177] An increase in blood–brain barrier permeability was observed in these animals,[176] suggesting a dose‐dependent relationship between SOD1 deficiency and neuronal susceptibility to oxidative insult.