Abstract

Despite the growing body of evidence indicating an increased risk of DAT following a TBI, the specific underlying pathology responsible for this risk remains a mystery. The majority of mechanistic explanations focus on a presumption of a neuropathologic trigger that is activated at the time of the injury and continues to evolve over time, eventually leading to dementia [1]. Axonal damage is a hallmark of both traumatic brain injury (TBI) and Alzheimer’s disease (AD), so many have looked into this possibility as a link between TBI and dementia. Amyloid-b (Ab), the primary protein most frequently associated with AD, has been shown to accumulate within neuronal cell bodies and injured axons within hours to days of TBI, according to human and animal models [2]. Amyloid precursor protein (APP) expression rises in injured axons and neuronal cell bodies in response to trauma, resulting in an increase in Ab production. It is hypothesized that this accumulation of APP and Ab plays a significant role in the subsequent Ab plaque formation, which is one of the hallmarks of AD. Additionally, it is hypothesized that the APOE 4 genotype may influence amyloid pathology and TBI outcome, putting individuals with this allele at increased risk for AD