Examining the brain of an NFL player who died at a relatively young age, a doctor found large deposits of “tau proteins.” In layman’s terms, these  are the equivalent of sludge in the engine of thought. They are believed to be caused by trauma.

Junior Seau was an All-Pro linebacker in the National Football League. He played most of his career in San Diego, where he became something of a cultural icon by being as likable off the field as he was dangerous upon it.

Professional football is a punishing occupation, and linebacker is one of its most punishing positions. Yet, Seau survived the violence and mayhem to play an astonishing 20 years before retiring in 2010.

Players do not become eligible for induction into the Hall of Fame until they have been retired for at least five years, so it was generally agreed the Charger great would enter the Hall in 2015 as a consensus first-ballot selection. It was unthinkable that an athlete of his stature would not be admitted at the earliest opportunity.

We now know that Junior will not be present in Canton, Ohio, when his memory is honored three years from now. He died last week at age 43, the victim of a self-inflicted gunshot wound to the heart.

When tragic events like this strike, we search for familiar narratives to make some sense of the inconceivable: The Greek god couldn’t adapt to life as an ordinary mortal. The very demons that fueled his competitive fire consumed him once the flame was extinguished. Deprived of the adulation of the crowd, maybe he drank too much, squandered his money, used drugs, suffered difficulties with women, yadda, yadda, yadda…

But as the powers that be in the NFL are only too well aware, there may be a more sinister explanation for this untimely death.   

Four days before the Seau tragedy, 62-year-old Ray Easterling was found dead of a gunshot in his Richmond, Va., home. He was a retired Atlanta Falcons’ safety and was undergoing treatment for dementia. Easterling was also one of more than 1,500 parties seeking class-action relief in federal court against the NFL and helmet maker, Riddell, on behalf of brain-damaged ex-players and their spouses.  His death was ruled a suicide.    

In February 2011, former Chicago Bears star Dave Duerson, 50, killed himself. He, like Seau, shot himself in the chest. Though most male gunshot suicides inflict head wounds, Duerson’s reason for not doing so was made clear in his final note to his family: “Please, see that my brain is given to the  NFL’s brain bank.” Even in death, the broken warrior sought to understand the source of his torment.

The NFL doesn’t have a brain bank, but the league did make a $1 million donation last year to Boston University’s Center for the Study of Traumatic Encephalopathy, after belatedly acknowledging that premature dementia was a possible side effect of playing professional football. That research group examined Duerson’s brain and reported he “had developed the same trauma-induced disease recently found in more than 20 deceased players.” (NY Times)

The October 2009 GQ magazine featured a lengthy article by Jeanne Marie Laskas entitled “Game Brain.” In it, the author related the saga of Dr. Bennet Omalu, the pathologist who discovered this "trauma-induced disease” while performing the autopsy of retired Pittsburgh Steelers’ center Mike Webster.

Though Webster’s brain appeared outwardly normal, microscopic examination revealed large deposits of “tau proteins” in its tissue. In layman’s terms, these proteins are the equivalent of sludge in the engine of thought. They are believed to be caused by trauma to the organ. Webster died at 50 with the brain of an advanced Alzheimer’s victim in his 90s.

Needless to say, the league was initially reluctant to attribute this phenomenon to football. But as Dr. Omalu began to acquire the brains of other former players who died young, the mounting evidence became clear enough to demand further study.

The early deaths were not necessarily the result of reckless and erratic behavior borne of some individual moral failing. Rather, the destructive life styles may have been the product of organic brain damage incurred on the so-called field of play.

Ironically, improved headgear may be responsible for much of the injury. The modern helmet does a terrific job of absorbing impact. That’s good news for the skull but bad news for the brain encased within it.

The brain is suspended in cerebral spinal fluid in the cranial cavity, tethered to the spinal column by its stem. When a player sustains violent impact to the head, this delicate structure slams into the interior of the skull, which can result in concussion.

The protective qualities of today’s helmets have, in effect, weaponized the head by immunizing it against external injury. Players can attack headfirst — a style of play that would be impossible without sophisticated helmets.

Of course, there are myriad unanswered questions about the syndrome. Unlike pugilistic dementia, affected brains exhibit no obvious contusions. There is also no Alzheimer-related shrinkage.

Why do some players lead normal lives after football while others crash and burn? Could steroid use play a role in the disease onset? These substances accelerate protein synthesis in muscle tissue. Could they also speed up tau protein production in the brain?

Are some persons genetically predisposed to the disorder? Are numerous minor concussions more harmful than one major injury? At the moment, there are no reliable solutions to these vexing riddles.

Borrowing a phrase from Friedrich Engels, we can say there is a specter haunting the National Football League. The origins and exact dimensions of the shadowy menace are difficult to gauge. Nonetheless, the threat is very real and it’s not going away anytime soon.