Most gene mutations associated with Alzheimers disease point to the metabolism of amyloid precursor protein as potential cause. The β- and γ-secretases are two executioners of amyloid precursor protein processing resulting in amyloid β. Significant progress has been made in the selective inhibition of both proteases, regardless of structural information for γ-secretase. Several peptidic and non-peptidic leads were identified and first drug candidates are in clinical trials. This review focuses on the developments since 2003.
Keywords: Alzheimer's disease, secretase, aspartic protease, inhibitor, presenilin
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