Abstract
Amyloid‐β (Aβ) is either directly involved in the pathogenesis of Alzheimer's disease (AD) or tightly correlated with other primary pathogenic factors. It is produced from amyloid precursor protein (APP) by proteolytic processing dependent on the β‐site APP‐cleaving enzyme 1 (BACE1) and γ‐secretase, and is degraded by a broad range of proteases. This update summarizes the currently available studies that have determined the usefulness of BACE1 and secreted fragments of APP and Aβ as cerebrospinal fluid biomarkers for AD.