Parallels between the redox properties and toxicity of Aβ in Alzheimer's disease and mutant Cu/Zn-SOD in familial amyotrophic lateral sclerosis

Abstract

Over the last decade, the pendulum of scientific opinion has swung towards the implication of β‐amyloid as the protein whose mismetabolism in linked to Alzheimer's disease. The factors that cause β‐amyloid accumulation, and the mechanism by which the peptide causes neuronal demise, are important for targeting therapeutics.