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Evidence accumulated over the past decades has shown that for many patients, traumatic brain injury (TBI) triggers cellular and molecular processes that continue to evolve long after the acute period and initial recovery. While these mechanisms result in short-term tissue repair and regeneration, the reparative process is often incomplete, and can also be maladaptive. Long-term outcomes after TBI are not fixed, but rather there can be improvement or deterioration years, even decades, after injury. TBI can result in long-term impairment and disability and increases risk of remote neurodegeneration and dementia. It is estimated that 5-10% of the population-wide burden of dementia is associated with TBI.
Despite the substantial societal burden imposed by long-term neurodegeneration and dementia after TBI, little is known about the underlying pathophysiological mechanisms of trauma-related neurodegeneration (TReND). For decades it was believed that TBI was associated with an increased risk for Alzheimer’s disease, but recent work indicates that other pathologies, including microvasculopathy, axonal degeneration, and neuroinflammation play prominent roles.
This presentation will review the epidemiologic data regarding TReND and will then discuss insights from neuropathologic studies on long-term survivors after TBI. Recent work using neuroimaging and molecular biomarkers measured years after TBI will be reviewed. Finally, we will discuss recent work pointing to potential therapeutic interventions.