The devastating deficiencies that result from brain injury stem from multiple overlapping mechanisms, exacerbated by the fact that there are no effective treatments. Traumatic brain injury (TBI) is recognized as the most influential environmental risk factor for neurodegenerative disease later in life, including dementia of Alzheimer’s disease (AD)-type. However, exactly how TBI triggers and strengthens the neurodegenerative cascade of events in AD remains controversial. Amyloid deposits and fibril precursor protein are extracellular in systemic amyloid A (AA) amyloidosis. In this chapter, I will discuss the neuropathology following TBI connected to AD. Additionally, I critically review recent animal and human studies regarding how brain trauma affects the potential risks factors for AD progression. Furthermore, it will be shown investigate the principal pathological features of dementia or AD, specifically focusing on axonal damage and consequent cleavage of the amyloid precursor protein (APP), amyloid β plaque formation, or phosphorylation and aggregation of tau, neurofibrillary tangles formation, and TDP-43 accumulation. In summary, despite recent progress more studies are required to (1) further understanding of the basic mechanisms and pathophysiology of TBI, (2) elucidate the precise association between TBI and neurodegenerative disease, and (3) to identify treatments and therapies that can mitigate long-term consequences.
- Amyloid beta
- Amyloid beta deposition