Abstract
The link between bio-metals, Alzheimer's disease (AD), and its associated protein, amyloid-β (Aβ), is very complex and one of the most studied aspects currently. Alzheimer's disease, a progressive neurodegenerative disease, is proposed to occurs due to the misfolding and aggregation of Aβ. Dyshomeostasis of metal ions and their interaction with Aβ has largely been implicated in AD. Copper plays a crucial role in amyloid-β toxicity, and AD development potentially occurs through direct interaction with the copper-binding motif of APP and different amino acid residues of Aβ. Previous reports suggest that high levels of copper accumulation in the AD brain result in modulation of toxic Aβ peptide levels, implicating the role of copper in the pathophysiology of AD. In this review, we explore the possible mode of copper ion interaction with Aβ, which accelerates the kinetics of fibril formation and promote amyloid-β mediated cell toxicity in Alzheimer's disease and the potential use of various copper chelators in the prevention of copper-mediated Aβ toxicity.
Short Twitter Statement: Authors explore copper ion interaction w/ Aβ and kinetics of fibril formation in promoting amyloid-β mediated cell toxicity in Alzheimer's disease and the potential use of copper chelators in the prevention of copper-mediated Aβ toxicity.
Authors explore copper ion interaction w/Aβ and kinetics of fibril formation in promoting amyloid-β mediated cell toxicity in Alzheimer's disease and the potential use of copper chelators in the prevention of copper-mediated Aβ toxicity.