APP and early-onset autosomal dominant Alzheimer disease: Wu et al. have reported that, through a series of signalling cascades, TBI results in the cleavage of both APP and tau (at APP N585a and Tau N368 sites, respectively), mediating Alzheimer’s disease pathogenesis through the promotion of Aβ production and tau hyperphosphorylation, processes which ultimately induce neuroinflammation and neurotoxicity [91].