CA2 and Alzheimer disease: Importantly, our data from AD mice are in line with the notion that an overall modulation of the Ca2+ machinery (i.e regulation of Ca2+-binding protein levels, Ca2+ channels, pumps or exchangers) in stressed dopaminergic neurons can be neuroprotective during mitochondrial insults (see for examples [121] for neuroprotection by the L-type Ca2+ channel blocker isradipine, [122] for neuroprotection by glutamatergic receptor antagonists; and also [123, 124]).