CD38 and early-onset autosomal dominant Alzheimer disease: By crossing the classical Alzheimer’s disease mouse model APPswePS1ΔE9 with CD38 KO mouse, Blacher et al. [64] found that CD38 deletion reduced Aβ plaque load and soluble Aβ levels, an effect that correlated with improved spatial learning in vivo and that was mimicked by inhibitors that blocked CD38 enzyme activity in vitro.