The neuropathologic basis of dementia in aging is a complex tapestry of misfolded proteins, vascular changes, and neurodegeneration that converge on the brains of persons with distinct genetic and ecologic backgrounds. Within this framework, it is perhaps unsurprising that neuropathologic understanding of dementia in aging individuals who played US football continues to evolve in complexity. Repetitive head impacts have been linked to chronic traumatic encephalopathy (CTE),1 a brain pathology later defined by the aggregation and stereotypic pattern of abnormally phosphorylated and misfolded tau protein.2 Other misfolded proteins commonly but not universally exist in brains with the pathologic characteristics of CTE, including ones (such as amyloid, transactive response DNA-binding protein [TDP] 43 kDa, and α-synuclein) that are observed in other age-associated dementias.3 Although vascular changes are among the most common and important pathologic features of the aging brain in Alzheimer dementia, and CTE is defined as a vasculocentric tauopathy,4 there is little known regarding the roles of conventional cerebrovascular disease pathways (eg, vessel disease, white matter changes, small infarcts) in the brains of persons with CTE and how these may or may not contribute to the likelihood of dementia.
Schneider JA. Multiple Pathologic Pathways to Dementia in Football Players With Chronic Traumatic Encephalopathy. JAMA Neurol. 2019;76(11):1283–1284. doi:10.1001/jamaneurol.2019.1089
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