Using a protein as a sponge to absorb the toxic plaque that builds up in the brains of Alzheimer's patients can halt symptoms and improve brain function, U.S. researchers suggest.

Scientists from the University of Rochester Medical Centre in Rochester, N.Y., performed studies on mice with a buildup of amyloid-beta, a toxic plaque that builds up in the brains of Alzheimer's sufferers and damages them.

This digital image of a brain is unlike that of an Alzheimer's patient, which is covered in a sticky plaque that interrupts and destroys normal functioning.
CBC

Their findings are published in an Aug. 12 online article in the journal Nature Medicine.

Instead of examining the mechanism that creates the excess plaque, scientists chose to focus on the protein that absorbs amyloid-beta in the body.

Known as soluble LRP (soluble low-density lipoprotein receptor-related protein), in healthy people, the protein binds to and neutralizes anywhere from 70 to 90 per cent of the amyloid-beta that is circulating in the body.

The scientists found that when they injected the mice with extra LRP, the body soaked up more amyloid and the brain also suddenly responded by significantly reducing levels of the substance.

The compound had an even more dramatic effect in mice with features of Alzheimer's disease: one type of LRP lowered the levels of amyloid-beta in their brains by 85 to 90 per cent.

The mice that received the compound also had improved learning and memory compared to mice that did not, and experienced 65 per cent more blood flow in their brains in response to brain stimulation.

"There is a dynamic equilibrium between the levels of amyloid-beta in the blood and in the brain," neuroscientist Berislav Zlokovic, the leader of the research team, said in a release.

"If we are able to lower the levels of amyloid-beta circulating in blood by sequestering more of it there, then the brain should follow and lower its levels too. This is exactly what we found."

Protein levels low in Alzheimer's patients

In the study, levels of soluble LRP in people with Alzheimer's were found to be about 30 per cent lower than in healthy people, and the soluble LRP that was present was almost three times as likely to be damaged compared to the same protein in healthy people.

Alzheimer's patients had on average three to four times as much loose, unbound amyloid-beta in their bloodstreams as people who didn't have the disease — high levels that would likely also be reflected in the brain.

The team is now working with a company called Socratech to create a form of LRP that could be tested in people. Zlokovic hopes to have such a product ready for testing within two years.

According to the Alzheimer Society of Canada, in 2007, an estimated 97,000 Canadians will develop Alzheimer's or another dementia-related disease, with 59,340 women and 37,870 men afflicted.

By 2011, the association predicts, new cases of dementia are expected to reach 111,430 per year.