Traumatic brain injury (TBI) is among the earliest illnesses described in human history and remains a major source of morbidity and mortality in the modern era. It is estimated that 2% of the US population lives with long-term disabilities due to a prior TBI, and incidence and prevalence rates are even higher in developing countries. One of the most feared long-term consequences of TBIs is dementia, as multiple epidemiologic studies show that experiencing a TBI in early or midlife is associated with an increased risk of dementia in late life. The best data indicate that moderate and severe TBIs increase risk of dementia between 2- and 4-fold. It is less clear whether mild TBIs such as brief concussions result in increased dementia risk, in part because mild head injuries are often not well documented and retrospective studies have recall bias. However, it has been observed for many years that multiple mild TBIs as experienced by professional boxers are associated with a high risk of chronic traumatic encephalopathy (CTE), a type of dementia with distinctive clinical and pathologic features. The recent recognition that CTE is common in retired professional football and hockey players has rekindled interest in this condition, as has the recognition that military personnel also experience high rates of mild TBIs and may have a similar syndrome. It is presently unknown whether dementia in TBI survivors is pathophysiologically similar to Alzheimer disease, CTE, or some other entity. Such information is critical for developing preventive and treatment strategies for a common cause of acquired dementia. Herein, we will review the epidemiologic data linking TBI and dementia, existing clinical and pathologic data, and will identify areas where future research is needed.
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Figure 1. Annual rate of traumatic brain injury–related hospitalizations and deaths, by age. Adapted from Faul et al.5
Figure 2. Histopathologic features of chronic traumatic encephalopathy in a former professional football player (courtesy of Ann McKee, MD, Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, Massachusetts). A, Scanning view of the hippocampus and parahippocampal cortex. Note intense immunostaining of the entire Ammon horn and subiculum with focal involvement at the depths of sulci of the inferior temporal lobe. B, Appearance of individual neurofibrillary tangles in the neocortex. C, Predilection for neurofibrillary tangle involvement in the superficial layers (layers II/III) (as opposed to deeper layers [layers V/VI], as is more common in Alzheimer disease) of the anterior insular cortex. D, Tendency for perivascular tau deposition and neurofibrillary tangle formation in the frontal cortex. All sections immunostained for abnormally phosphorylated tau (AT-8, monoclonal antibody that detects hyperphosphorylated tau, serine 202, and threonine 205). A, Original magnification ×1. B, Original magnification ×160. C, Original magnification ×30. D, Original magnification ×60.
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