Traumatic Brain Injury and Alzheimer’s Disease: Exploring the Pathological Overlap and Risk of Neurodegeneration

Abstract

Traumatic brain injury (TBI), particularly repetitive mild TBI, has emerged as a significant risk factor for the development of Alzheimer’s disease (AD)-like pathology. Neuropathological studies have identified shared features between TBI and AD, such as amyloid-beta (Aβ) deposition and hyperphosphorylated tau (p-tau) aggregates. However, distinct regional patterns differentiate chronic traumatic encephalopathy (CTE) from AD, making the relationship between TBI and neurodegenerative diseases a complex and debated issue. Diagnostic challenges are compounded by overlapping clinical symptoms and the limitations of current imaging and biomarker techniques, which hinder precise differentiation between TBI-associated neurodegeneration and classical AD. Despite these challenges, recent advances in tau-specific imaging technologies and blood-based biomarkers hold promise for enhancing diagnostic accuracy and distinguishing TBI-related changes from AD pathology. This study aims to enhance the understanding of the mechanisms linking TBI and AD by examining shared and distinct pathological features. It explores how TBI may trigger or accelerate neurodegenerative processes leading to AD-like pathology. By focusing on amyloid-beta and tau patterns in TBI, we aim to clarify the role of TBI in AD development and identify potential biomarkers for early detection and intervention. The study also emphasizes the need for longitudinal research and personalized therapeutic strategies to mitigate TBI's long-term effects on brain health.