Abstract
Traumatic brain injury (TBI) has emerged as a critical environmental risk factor for the development of frontotemporal dementia (FTD), a neurodegenerative disorder characterized by progressive declines in executive function, behavior, and language. While the acute symptoms of head trauma often resolve, the long-term neurological consequences can include a significant increase in FTD susceptibility. A comprehensive search of electronic databases, including PubMed and Google Scholar, was conducted to identify relevant peer-reviewed studies published through 2026. This review examines the complex pathological mechanisms linking blunt force trauma to frontotemporal degeneration, specifically focusing on the role of traumatic axonal injury (TAI) and the subsequent accumulation of beta-amyloid plaques alongside related FTD-associated proteinopathies.