for Alzheimer disease (AD). The A539T substitution in BChE-K is located at the C terminus,
which is essential both for BChE tetramerization and for its capacity to attenuate β-amyloid
(Aβ) fibril formation. Here, we report that BChE-K is inherently unstable as compared with
the" usual" BChE (BChE-U), resulting in reduced hydrolytic activity and predicting prolonged
acetylcholine maintenance and protection from AD. A synthetic peptide derived from the C …