APP and Alzheimer disease: Recent studies indicate that promoting the non-amyloidogenic processing of accumulated APP by soluble APP alpha (sAPPα) administration (Corrigan et al., 2012b), increasing AB CA1 levels (Loane et al., 2011) and inhibiting c-JNK (Rehman et al., 2018) reduced Aβ pathology further suggesting a role for Aβ accumulation in AD pathogenesis post-TBI.