In addition, axonal swellings filled with APP, suggestive of impaired axonal transport, are a well-documented morphological phenotype within injured regions of the brain and serve as a pathological marker for TBI-induced axonal damage.4 Previous studies suggest that altered amyloidogenic processing of APP and impaired APP axonal transport are interlinked, and both have been proposed as phenomena underlying generalized AD initiation and progression.5 However, whether and how these cellular processes are affected in human neurons following mTBI remains unexplored. This evidence concerns the gene APP and Alzheimer disease.