For more than a decade, researchers trying to make sense of the mysterious degenerative brain disease afflicting football players and other athletes have focused on the threat posed by concussions. But new research suggests that attention was misguided.

Instead of concerning themselves with the dramatic collisions that cause players to become dizzy, disoriented or even lose consciousness, neuroscientists should be paying attention to the routine hits to the head, according to a study that examines the root cause of chronic traumatic encephalopathy, better known as CTE.

“On the football field, we’re paying attention to the bright, shiny object — concussion — because it’s obvious,” said Dr. Lee Goldstein of Boston University, who led the study published in the journal Brain. But, he continued, “it’s hits to the head that cause CTE.”

The disease is marked by abnormal deposits of calcium and proteins in the brain, as well as by neuropsychiatric symptoms ranging from tremors and memory problems to depression and rage. The only way to diagnose it is by examining brain tissue after death.

Some of the hits that cause CTE may result in concussion, Goldstein said. But his team’s findings show that concussion is not necessary to trigger the process. Indeed, the new research suggests that concussion and CTE are completely different medical problems.

In mice, head impacts that caused concussion and those that led to CTE had different effects inside the brain. In people, the symptoms tend to show up as different behaviors that became evident at very different times. In mice, the research found immediate behavioral responses to head impact that ranged from zero to disability. And researchers captured what appeared to be the earliest moments of CTE in many mice that showed few if any immediate symptoms.

That new research underscores that the kinds of “sub-concussive” blows to the head that many athletes routinely endure are far more worrisome than players, their parents and their physicians have been led to believe.

Even as football programs adjust rules to reduce concussions, the findings suggest the efforts will not be enough to prevent long-term injury.

“You have to prevent head impact,” Goldstein said.

The new work originated at Boston University’s Center for Chronic Traumatic Encephalopathy and drew in dozens of experts from a wide range of disciplines and institutions.

The team began by inspecting the brains of four teenage athletes who died one day, two days, 10 days and four months after serious head injuries. Those brains were compared with others belonging to teen athletes who died without a history of head injury.

The researchers observed an abnormal buildup of a protein called tau — a hallmark of CTE — in two of the athletes who experienced head trauma. One, in fact, met the diagnostic criteria for early CTE.

That and other evidence led the researchers to hypothesize that early CTE may result from leaky blood vessels in the brain. In the deep recesses of the organ’s folds, these damaged blood vessels were letting proteins spill into nearby brain tissue, triggering inflammation, they surmised.

To see whether they were right, they needed to study a population of subjects with greater rigor. So they built a machine to deliver calibrated blows to young male mice, subjecting them to a range of head impacts. The effects of these blows were recorded in imaging scanners, in test mazes and on pathology slides.

The researchers examined the animals’ brain chemistry, cortical structure and behavior. They performed computer simulations to repeat and extend their findings on how various brain tissues responded to head impacts.

Delivered a powerful blow, some mice would reel from the injury for days but then recover. Upon dissection, their brains might even look fine.

Other mice, including many who got a series of blows equivalent to participating in a single game or practice, would behave normally in the days following a head impact. But not much later, their brains would reveal early signs of tau protein accumulations.

These deposits appeared to start in the deep recesses of the brain’s folds, where the hallmarks of full-fledged CTE are most clearly seen in humans.

The results may explain why approximately 20 percent of athletes who were found to have CTE after they died had never received a concussion diagnosis, Goldstein said. And they suggest that people who seem to bounce back after getting their “bell rung” may well have sustained damage that will not be evident for years.

“The overwhelming majority of people whose brains are hurt are going right back in and doing the worst thing possible: getting hit again and again,” Goldstein said.