SOD1 and amyotrophic lateral sclerosis: We recently proposed that biochemical similarities between vulnerable neuronal populations in ALS and Parkinson's disease promote the evolution of a shared detrimental biomolecular cascade, within which misfolded SOD1 constitutes a key therapeutic target.[166b] Spinal cord motor neurons[210] and SNc dopamine neurons are prone to mild redox dyshomeostasis, mitochondrial dysfunction and protein misfolding during healthy aging,[166b] which become progressively exacerbated by additional pathogenic factors such as genetic mutations, biometal dysregulation (Cu, Fe) or exposure to toxins.