For example, within 24 hours of mild TBI in mice, reductions in mitochondrial membrane potential are accompanied by increased calcium retention and upregulation of NCLX (Na/Li/Ca exchanger) to mitigate calcium overload [52], while Aβ concurrently impairs calcium uptake, compromising buffering capacity, as shown in vitro with oligomeric Aβ1–42 and in transgenic amyloidosis mouse models [53–55]. This evidence concerns the gene SLC8B1 and amyloidosis.