Systems and methods for inhibiting γ-secretase production of amyloid-β peptides

Abstract

Inhibitors are provided for targeting γ-secretase to reduce amyloid load as a viable strategy in Alzheimer's disease treatment and drug discovery. γ-secretase has been shown to cleave amyloid precursor protein, causing an increase in extracellular concentration of amyloid-β peptides. This extracellular concentration increase can lead to build-up amyloid plaques in patients and associated health complications for them. The inhibitors bind to a C-terminal lysine cluster adjacent the transmembrane domain of amyloid precursor protein through both covalent and non-covalent interactions. These interactions inhibit the ability of γ-secretase to cleave the amyloid precursor protein, halting the build-up of extracellular amyloid-β peptides. The inhibitors exhibit specificity for amyloid precursor proteins, reducing concerns of potential off-target effects.

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