Abstract
The progression of Aβ peptide aggregation in the brain has been suggested to play an important role in the pathogenesis and development of Alzheimer’s disease. The present study is intended to provide insight into the interactions between the zinc binding site of beta-amyloids and the zinc ion itself. It has been amply demonstrated that the absence of zinc bonded to the beta-amyloid may slow down the progression of the Alzheimer disease, so the goal is to provide an analysis of available drugs that can be repurposed, while waiting for the development of novel therapeutics. To this end, we address the issues of how and with what strength the existing compounds bind with beta-amyloid, potentially replacing or blocking zinc and preventing it from attaching to the amyloid itself. The analysis was performed using MOE software which, starting from a filtered database, made it possible to identify the drugs that were most likely to bind to the zinc binding site on beta-amyloid.
Published Version
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