Age at injury influences dementia risk after TBI

Abstract

Traumatic brain injury (TBI) is increasingly recognized as a risk factor for dementia. New data provide further support for this association, and demonstrate the influence of age at injury and injury severity on dementia risk post-TBI; revealing that even mild TBI increases dementia risk in those aged ≥65 years. The association between traumatic brain injury (TBI) and increased risk of dementia has garnered intense public and media interest in the past few years. In a newly published, comprehensive study of 164,611 patients with trauma aged ≥55 years at the time of injury, the strength of this association is explored further 1 ; the results highlighting the influence of age on dementia risk following a TBI. In support of previous work, Gardner and colleagues 1 report an increased dementia risk following a single moderate to severe TBI across their patient cohort at up to 7 years of follow-up. Furthermore, an intriguing aspect of the analysis indicates that even a single, mild TBI might confer increased dementia risk in older patients; defined as those aged ≥65 at the time of injury. Thus, the implications of this study are that risk of neurodegeneration after TBI is influenced not just by the severity of the initial injury, but also by the patient's age at the time of injury. In the past 5 years considerable attention has been paid to the link between repetitive, mild TBI and neurodegenerative disease. This interest has, in large part, been driven by increasing reports of chronic traumatic encephalopathy (CTE) in autopsy studies of former athletes or military personnel. 2,3 However, the association between exposure to a single moderate or severe TBI and increased risk of dementia has been recognized for some time. Characterization of autopsy acquired material from long-term survivors of a single TBI reveals a complex neuropathology in a proportion of patients. This complex neuropathology, best described as a 'polypathology', includes abnormal tau and amyloid-β protein accumulation, 4 neuroinflammation, white matter degradation and axonal degeneration, 5 adding further to our appreciation of the full range of CTE pathology.