Brain injury study adds to Alzheimer's enigma

CHICAGO (Reuters) - Levels of a protein linked with Alzheimer's disease rise as people recover from brain injuries -- a surprising finding that may help explain why injuries boost the risk of developing the disease, U.S. and Italian researchers said on Thursday.

Researchers at Washington University in St. Louis and the University of Milan did hour-by-hour measurements of the protein amyloid beta in 18 patients with severe brain injury as they were coming out of a coma.

"We were trying to understand why traumatic brain injury increases the risk of Alzheimer's disease," said Dr. David Brody of Washington University, whose research appears in the journal Science.

Brody said people with severe brain injuries have a two to four times greater risk of developing Alzheimer's disease.

One theory is that such injuries increase the amount of amyloid beta, which may accelerate the development of sticky clumps of amyloid plaque that is a hallmark of Alzheimer's disease.

To study this, the teams placed a small catheter into the brains of the patients to sample fluid in the spaces between cells, where amyloid beta protein accumulates.

Then, they took hourly measurements of the fluid to check levels of the protein.

"What we were expecting was that amyloid beta levels would be high immediately after the injury and fall over time," Brody said in a telephone interview.

What they saw instead was a gradual increase in levels of this protein as patients recovered brain function. The better the patients got, the higher their amyloid beta levels rose. And in patients whose neurological function worsened, amyloid beta fell.

Brody said the finding suggests that amyloid beta in the human brain may be an indicator of how well brain cells are communicating, something studies in mice have suggested.

And while it also proves it is possible to directly measure amyloid beta in humans, "it raises a lot more questions than it answers," Brody said.

Alzheimer's disease researchers are trying to find out whether drugs that remove amyloid plaque will slow the progression of the disease.

While the study measured total soluble amyloid beta in the fluid between the cells, it likely missed any amyloid inside of cells, Brody said. And their measurements may not have been sensitive enough.

"This study is just the beginning," Brody said.

Alzheimer's is the most common form of dementia, affecting 5.2 million people in the United States and 26 million globally, according to the Alzheimer's Association.

(Editing by Maggie Fox and Xavier Briand)