WASHINGTON — Scientists for the first time have peered into people’s brains to directly measure the ebb and flow of a substance notorious for its role in Alzheimer’s disease.

The delicate research was performed not with Alzheimer’s patients but with people suffering severe brain injuries — because a brain injury increases the risk of developing dementia later in life.

The goal is to learn why, so that doctors one day might be able to lower that risk

But with this first-step study, a team of scientists from Missouri and Italy got a surprise.

Too much of that Alzheimer’s-related protein, called beta-amyloid, is thought to be harmful. So the team had expected beta-amyloid levels to spike right after the injury and then drop as patients recovered.

Instead, beta-amyloid levels increased as patients improved and dropped if they got worse, the lead researcher, Dr. David Brody, a neurologist at Washington University in St. Louis, reported Friday in the journal Science.

What’s going on? Beta-amyloid seems to be a marker of increased brain activity as patients improved.

If so, what started as a study of Alzheimer’s risk might have implications for how the brain-injured are tracked in intensive-care units — although that will take much more research to prove.

“Our study is just the beginning,” Dr. Brody said. “Amyloid-beta measurements in the brain may turn out to be a good indicator of how well the cells are communicating with each other.”

Beta-amyloid is best known as the sticky goo that makes up the hallmark plaques inside the brains of Alzheimer’s victims. But it doesn’t start out as gunk. Soluble forms are found in the fluid that bathes the brain, although scientists don’t understand its purpose, or just what happens to trigger formation of those bad plaques.

While the work raises more questions than it answers, it brings researchers a valuable new tool for studying both Alzheimer’s risk and just what happens during brain-injury recovery.