Zinc, Amyloid beta, Alzheimer's disease, trace metals, brain, proteostasis
Protein aggregation is a cornerstone in amyloid-forming neurodegenerative diseases that is largely due to altered conditions in the biochemistry of key components of the neuronal environment, including metal ions. Indeed, trace neurometals such as calcium, zinc, and copper are vital players in brain neurobiology, whose homeostasis is altered in most neurodegenerative conditions; further, metals ions are widely found within proteinaceous inclusions from patients and animal models. This chapter briefly gives an overview of the influence of trace metals in amyloid formation in connection to their homeostasis in the brain. In particular, the role of zinc in Alzheimer’s disease is more thoroughly discussed. Indeed, the deregulation of zinc ions has well-established mechanistic links to Alzheimer’s pathophysiology, including direct interaction effects with amyloid β and tau, the two amyloid-forming proteins involved in this neurodegenerative disease.