With three recent studies linking concussions to future degenerative brain diseases, there’s one big question that combat vets, athletes and other brain-injury victims have to be asking themselves: “What may happen to our brains?”

It’s a critical question because we have to know how this disorder develops in order to know how to prevent it from progressing.

Unfortunately, all we have are theories at this time. But they are at least a starting point.

John Medina, author of the best-selling book, “Brain Rules,” has written extensively about some of the theories of chronic traumatic encephalopathy (CTE), and much of this column will be devoted to summarizing his findings in a 13-part series of posts on his blog site “Brainstorm”: http://blog.spu.edu/brainstorm/

Originally, we believed that the original brain injury was the cause of CTE. When our brains are shaken by roadside bombs in Iraq or head-on collisions with an oncoming linebacker, there is damage because the inside of our skull is just as hard as the outside.  Nerve tissue is sheared by the blow or scraped against the inside of the skull, causing permanent damage.

But even permanent damage doesn’t explain the progressive nature of CTE, starting with headaches and leading to cognitive impairment and ultimately to dementia and death. What’s causing that?

One of the hallmarks of CTE is that the brain contains tangled knots of a protein called tau. This protein is a normal component of neurons. In fact, it has been compared to a food supply line that provides nutrients to the brain cells. When the supply line is interrupted, according to one theory, the brain cells begin to die from lack of nutrition.

But tau has another function, which is holding together the cell walls of neurons. When the tau begins to lump up, the cells walls lose their form and begin to collapse, then to leak. That allows a salty brine outside the neuron to invade the cells, damaging and ultimately killing them, according to a second theory.

A third theory involves a specialized group of cells called microglial cells. These are damage control officers that can migrate around your entire brain searching out problems like foreign organisms, damaged cells or localized injuries.  Then they provide damage control by unleashing a whole host of chemical molecules, some of which destroy the invaders and some of which promote healing.  However, the problem comes with the repeated injuries, according to this theory. The microglial cells, which had been partially activated from a previous injury, spring into action again and again. Finally, they adapt to repeated injuries by remaining partially activated all the time, a status known as “priming.”  This may be a part of degenerative brain diseases.

Finally, a fourth theory involves mitochondria, the tiny energy centers within each brain cell. There’s some speculation that when the cells begin to leak after an injury, calcium comes seeping in. Mitochondria, which are tiny beanlike structures surrounding the cell’s nucleus and dotting its cell walls, begin trying to eat the calcium until they eventually fill up and pop. Without those tiny energy centers (you could think of them as batteries), the cell begins to die.

Obviously, researchers have much more work to be done. CTE could be a result of any of these processes, it could be a combination of any or all of them, or it could be a new mechanical function that we haven’t recognized yet.

So that complicates the next – and most critical – question: What, if anything, can we do to prevent CTE from progressing?