The abnormal accumulation of β-amyloid (Aβ) in the brain is an early and invariant feature in
Alzheimer's disease (AD) and is believed to play a pivotal role in the etiology and
pathogenesis of the disease. As such, a major focus of AD research has been the
elucidation of the mechanisms responsible for the generation of Aβ. As with any peptide,
however, the degree of Aβ accumulation is dependent not only on its production but also on
its removal. In cell-based and in vitro models we have previously characterized endothelin …