This is from Boston University. They have isolated a "tau protein" in these players.

Chronic Traumatic Encephalopathy (CTE) (click here) is a progressive degenerative disease of the brain found in athletes (and others) with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head. CTE has been known to affect boxers since the 1920s. However, recent reports have been published of neuropathologically confirmed CTE in retired professional football players and other athletes who have a history of repetitive brain trauma. This trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau.  These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement.  The brain degeneration is associated with memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia....

Tau proteins  are proteins that stabilize microtubules. They are abundant in neurons of the central nervous system and are less common elsewhere, but are also expressed at very low levels in CNS astrocytes and oligodendrocytes.

Microtubules support cellular processes. The tau proteins are found, in my opinion, in higher numbers in the brains of former football players because the tissue has been damaged. These proteins are probably at first released outside of the cells due to damage and then continue to function, but, now function inappropriately causing greater damage. That is pure theory, but, it seems to me to be realistic. 

So, the question arises as to how to 'turn off' these dysfunctional proteins without turning them off while they function properly. Research. We need to understand what happens to 'advance' the deterioration after the initial injury. 

To date, (click here) the only established function of Tau is the promotion of assembly of tubulin into microtubules and stabilization of their structure. The protein occurs mainly in the axons of the CNS and consists largely of six isoforms generated by alternative splicing; the longest of them has 441 amino acids....