Being published Monday by Boston University School of Medicine researchers, the study reports on the autopsies of 85 brain donors, most of them professional athletes. It comes as concerns mount over the dangers of head injuries in contact sports and some call for banning tackle football for younger children.

The work provides new insight into an Alzheimer’s-like condition, called chronic traumatic encephalopathy, that is thought to be caused by repeat concussions or blows to the head. The autopsies revealed extensive evidence of protein tangles called tau clogging brain tissue and causing the destruction of brain cells in football players, wrestlers, hockey players, boxers, and military veterans who served in combat zones.

“The sheer size of our study should make any doubters no longer doubt” that CTE is a real condition caused by repeat head injuries, said study co-author Dr. Robert Cantu, a neurosurgeon and co-director of the BU Center for the Study of Traumatic Encephalopathy.

These findings could prove helpful to the mega lawsuit against the National Football League filed last spring by thousands of former players and their families, who claim that the National Football League hid information that linked football-related head injuries to dementia, depression, and other cognitive problems. It also underscores the potential dangers of youth football, months after a September Pop Warner game played in Central Massachusetts resulted in five concussions for 10- to 12-year olds.

Some neurologists, however, emphasized that there’s still reason for skepticism about whether multiple blows to the head really do lead to tau tangles. “Yes we can all agree now that this is a real brain condition, but we don’t all agree on whether multiple concussions cause the emergence of this entity,” said Peter Warinner, director of sports neurology at Brigham and Women’s Hospital who heard the study findings presented at a recent research conference in Switzerland.

The researchers reported in the journal Brain that 68 of the 85 individuals they examined, all of whom had experienced repeated head trauma, had evidence of CTE. But they cautioned that the study was not designed to establish the frequency of this type of brain damage in athletes. They didn’t see any signs of tau in the brains of 18 controls, who were matched by age and had never experienced concussions or other brain injuries.

Symptoms of CTE were first described in retired boxers in the 1920s and have been documented in football players, hockey players, boxers, military veterans, and those with a predilection for head banging. While the condition hasn’t been found in the brains of those without head trauma, Warinner said that could simply be due to the fact that it’s rare and that more brains in the general population need to be autopsied.

The new study described four stages of the disease, noting that symptoms can progress for years after head trauma. It starts with headaches and problems with concentration in the early stages, followed by depression, aggression, explosive anger and short-term memory loss. Then comes more serious cognitive impairment, and eventually full-blown dementia where a person doesn’t recognize loved ones.

Athletes and military veterans who experienced such symptoms before they died donated their brains for further research. “We’re not studying a group that went on to live productive lives after their football or military careers,” said Cantu. “Those who decide to have their family member’s brain studied want to figure out what went wrong near the end of his life.”

Study leader Dr. Ann McKee, a BU neurologist who directs the Bedford VA Medical Center brain banks used for the study, said certain genetic factors most likely combine with the number and severity of head blows through a person’s lifetime to determine the likelihood of developing the condition, which has no treatment and no diagnostic test beyond an autopsy.