Maintaining metal ion homeostasis is essential for diverse cellular processes, particularly in the central nervous system. Changes to the transition metals, copper, zinc, and iron in Alzheimer’s disease (AD) have been extensively reported, especially in the brain, blood, and cerebrospinal fluid. Through interactions with disease-associated proteins, including amyloid precursor protein, the proteolytically cleaved peptide amyloid-beta (Aβ), and tau, these biometals play an important role in disease pathogenesis. Currently, no disease modifying therapy exists for AD and clinical trials over the past decade aimed at targeting established disease mechanisms have failed to alter disease progression. Targeting biometals in AD by restoring metal ion homeostasis represents an alternative potential therapeutic avenue.
Biometals in Neurodegenerative Diseases, Mechanisms and Therapeutics, 2017, Pages 1-17,