NGB and Alzheimer disease: Although it would seem logical to attempt to confirm the relevance of Ngb in the prevention of AD phenotype by crossing the hAPP NL/F mice with Ngb KO mice (Hundahl et al., 2012), these mice do not present abnormalities in anatomy, neuronal loss, body composition or behavior, implying that Ngb physiological (protective) roles can be efficiently compensated when missing constitutively by any of the multiple survival mechanisms present in neurons (Hundahl et al., 2011, 2012).