PTH and chronic kidney disease: To facilitate this drug repurposing, future studies will be required to confirm Aβ42 neutralization as the operative mechanism for the PTH suppressive response to aducanumab or other similar biologic agents, define the nature of Aβ42 suppressive interactions with calcimimetic compounds on PTH end organ targets, and conduct careful evaluation of the action of these compounds in other pathophysiological contexts such as chronic renal failure where additional tools for medical management of PTH hypersecretion would be especially useful.