Moreover, TBI-dependent amyloid or tau pathologies have been less reliably demonstrated in models of mild or repetitive mTBI, despite the use of mice expressing human amyloid precursor protein or tau proteins,107 and any persistence or progression of these pathologies after injury(s) has rarely been demonstrated.78,106 This is in striking contrast to human TReND, which is typically identified years after injury.21 Moreover, animal models also do not reflect associated features of tau pathology, such as transactive response DNA binding protein 43 (TDP-43) immunoreactive nuclear inclusions. This evidence concerns the gene TARDBP and amyloidosis.