Figure 1

The empirical data regarding tauopathy and contact sports appear to indicate that certain contact sports may be associated with an altered distribution of phosphorylated tau when examined at autopsy years to decades following sports participation. The significance of this change and the correlation between such changes and clinical signs are matters of considerable uncertainty, as more research with more rigorous prevalence data is necessary even for this preliminary assertion. This is in contrast, however, to the accepted paradigm, none of which has been objectively demonstrated in humans. The accepted paradigm indicates that head trauma per se and in particular concussion, initiates the overall process, which in turn sets in motion neuroinflammatory processes that span a large spectrum of biology. Phosphorylation of tau via pathological alteration of kinase-phosphatase equilibrium subsequently occurs in brain regions vulnerable to mechanical stress. Soluble, low-n phospho-tau oligomers of altered conformation or ‘strain’ then spread along neuroanatomical pathways, effect conformational changes in other phospho-tau species via protein templating, and cause trans-synaptic neurotoxicity, which fosters disease progression. The tendency for frontotemporal involvement by phosphorylated tau further is suggested to be the basis for complex behaviors, such as impulse control, mood, and attention, as well as the reported psychiatric manifestations of CTE. Involvement of memory pathways is suggested to disrupt episodic memory. The overall neurotoxic cascade is said to overlap with, include, or even cause, pathology of Alzheimer’s disease, frontotemporal lobar degeneration, and/or amyotrophic lateral sclerosis.