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Astrocytes may not only be involved in the clearance of Amyloid beta peptides (Aβ) in Alzheimer's disease (AD), but appear to produce N-terminally truncated Aβ (Aβn-x) independently of BACE1, which generates the N-Terminus of Aβ starting with Asp1 (Aβ1-x). A candidate protease for the generation of Aβn-x is cathepsin B (Cat, especially since CatB has also been reported to degrade Aβ, which could explain the opposite roles of astrocytes in AD. In this study, we investigated the influence of CatB inhibitors and the deletion of the gene e

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