Some proteins implicated in neurodegeneration/Aβ-pathology have important developmental functions.29,30 Atypical neurodevelopmental trajectories have been described in carriers of SORL1 risk variants,16 and there is evidence for increased proliferation of NPCs in mice lacking Sorla.31 In addition, to being key to neurodevelopment, recent studies have shown that NPCs and hippocampal neurogenesis persist beyond 90 years of age in Alzheimer’s disease cases.32,33 Hippocampal neurogenesis declined with age, with the extent of decline being correlated with disease severity. This evidence concerns the gene SORL1 and early-onset autosomal dominant Alzheimer disease.