Cathepsin B degrades amyloid-β in mice expressing wild-type human amyloid precursor protein.

Abstract excerpt

Accumulation of amyloid-β (Aβ), believed to be a key trigger of Alzheimer disease (AD), could result from impaired clearance mechanisms. Previously, we showed that the cysteine protease cathepsin B (CatB) degrades Aβ, most likely by C-terminal truncation, in mice expressing human amyloid precursor protein with familial AD-linked mutations (hAPP(FAD)). In addition, the Aβ-degrading activity of CatB is inhibited by...

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