Elevated cerebral levels of amyloid β-protein occur universally in Alzheimer's disease, yet
only a few patients show evidence of increased Aβ production. Therefore, defects in
proteases that degrade Aβ could underlie some or many cases of familial and sporadic AD.
This previously neglected topic has begun receiving serious attention. Understanding how
proteolysis regulates Aβ levels in the cerebral cortex has implications for both the
pathogenesis and the treatment of this protean disorder.