Traumatic brain injury and neurodegenerative diseases: the role of axonal injury and amyloid-β

Abstract

Traumatic brain injury (TBI) often leads to neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), imposing a substantial global disease burden. However, the underlying mechanistic link remains elusive. Recent research highlights the critical role of traumatic axonal injury (TAI) in TBI-induced Alzheimer’s disease. TAI disrupts axonal transport, leading to the pathological accumulation of proteins such as amyloid precursor protein (APP) and its cleavage product amyloid-beta (Aβ). These disruptions contribute to neurodegenerative processes in Alzheimer’s disease, including the formation of Aβ oligomers and plaques, which produce neurotoxicity. This review summarizes recent advancements in understanding these pathophysiological processes and underscores novel insights and methodologies for post-traumatic Alzheimer’s disease. The implications of these findings for future research and clinical significance are also discussed.