CASR and Alzheimer disease: Apart from the transient overexpression of the CaSR in NAHAs and the progressive overexpression in the hippocampal astrocytes and neurons of 3 × Tg AD-model mice [20,39], this interaction drives the surplus production, accumulation, and secretion of Aβ42 and hyperphosphorylated Tau oligomers from both NAHAs and neurons, coupled with increased cell death among the latter.