APP alterations result in the aggregation of Aβ fibrils that form plaques, and oligomers thought to induce neurotoxicity and promote formation of tau protein neurofibrillary tangles.9In vivo measurement of Aβ shows that as plaque deposits increase, cerebrospinal fluid (CSF) Aβ decreases.10 Studies of TBI brains at autopsy provide evidence for aberrant APP processing,11,12 raising the possibility that increased risk for AD following TBI is related to exacerbation of the primary neuropathology of AD. Here, APP is linked to Alzheimer disease.