Aside from direct oxidative stress‐induced neuronal damage, the disruption of redox homeostasis within vulnerable neuronal populations may also contribute to neuron death by exacerbating other detrimental cellular pathologies, including Aβ plaque formation in Alzheimer's disease[167a, 167b] and α‐synuclein deposition in Parkinson's disease.[166b] In this way, SOD1 dysfunction may constitute a modulator of disease progression, rather than an initial trigger for neurodegeneration, in some neurodegenerative disorders. Here, SOD1 is linked to Alzheimer disease.