Amyloid-beta is a thinking brain’s protein. A new study involving people with severe brain injuries shows that as neuronal activity increases, levels of amyloid-beta in the brain also go up.

A-beta, as the protein is sometimes called, is best known for causing plaques in the brains of people with Alzheimer’s disease. It is a normal component of the brain, but scientists don’t know what it does.

Traumatic brain injuries increase the risk for Alzheimer’s disease. So to find out if brain injuries cause a spike in amyloid-beta levels that could lead to plaque formation, a team of researchers from Milan, Italy, and Washington University in St. Louis sampled fluid from the brains of 18 comatose patients. The researchers inserted devices in the patients’ brains to monitor pressure. A small catheter sipped up fluid that gathers between brain cells, and then the researchers tested the fluid for A-beta.

What the researchers found was exactly the opposite of what they expected, says David L. Brody, a neurologist at Washington University who led the study with Sandra Magnoni of the Ospedale Maggiore in Milan. Instead of seeing a spike of A-beta soon after brain injury from falls, car accidents, assaults or hemorrhages, levels of the protein started low and rose as the patients improved, the team reports in the Aug. 29 Science.

“This is a fantastic study using an extraordinarily powerful technique to study human physiology and pathophysiology,” says Bradley Hyman, director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital and Harvard Medical School in Boston. “While the implications for a ‘normal’ function of A-beta are intriguing, it is still not completely clear whether the data reflect an active role for A-beta or simply establish that it is a marker for neuronal activity. Sorting this out will be fascinating.”

The results are consistent with previous studies in mice that show that A-beta is a byproduct of brain cell activity, and with studies in people that show the areas of the brain that are most active are the most prone to developing Alzheimer’s plaques, says John Cirrito, a neuroscientist at Washington University who established the link between brain cell activity and A-beta in mice but was not involved in the new study. A-beta may become a tool for monitoring brain activity in comatose patients, Cirrito suggests.

But the findings seem to contrast with preliminary results from a similar study in Sweden. Neurologist Lars Hillered at Uppsala University Hospital sampled brain fluid from eight comatose patients and found that people with diffuse brain injuries had higher levels of amyloid-beta in their brains.

“It could be that we’re onto something similar,” Hillered says. Electrical activity in brain cells and damage to cells may both raise levels of A-beta, he says.

Fluid taken by spinal tap doesn’t show the link between A-beta levels and brain activity. That is probably because the brain fluid the researchers sampled for the study came directly from the space between brain cells, while cerebral spinal fluid contains proteins filtered from blood as well as from the brain, Brody says.

Researchers still don’t know why brain injury puts people at higher risk for Alzheimer’s disease or what the protein’s normal job is in the brain.

“This study raises more questions than it answers,” Brody says. “It’s really just the beginning.”

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Found in: Body & Brain