From Washington, D.C., at the Experimental Biology 2007 meeting
Despite memory-test and brain-imaging advances in recent years, diagnosis of Alzheimer’s disease remains a challenge. Usually, only the presence of clumps of the protein amyloid-beta in the brain at autopsy confirms that a person’s dementia was Alzheimer’s. A study in mice, however, suggests that a test for excess amyloid-beta in the blood could signal Alzheimer’s even before any symptoms show up.
If the scientists can adapt the test for use in people, Alzheimer’s screening might someday identify individuals eligible for preventive therapies, says Stina M. Tucker of the Johns Hopkins University School of Medicine in Baltimore. Such therapies, now under development, would slow the body’s amyloid-beta production or clear the proteins from the brain before cognitive impairment occurs.
The new test is based on antibodies that bind to the amyloid-beta proteins. After Tucker’s Johns Hopkins colleague Juan C. Troncoso created the mouse antibodies, the researchers devised a way to use them to quantify amyloid-beta in a mouse’s blood.
The scientists injected the antibodies into mice, then several hours later drew blood, filtered out the antibodies, and measured the amount of amyloid-beta collected.
The researchers worked with healthy, normal mice and with animals genetically engineered to produce amyloid-beta to model human Alzheimer’s disease. The normal mice showed no excess amyloid-beta protein in their blood, but neither did engineered mice that had already developed moderate-to-advanced amyloid-beta clumps in their brains.
Only engineered mice with beginning Alzheimer’s-like disease had excess protein in their blood. Tucker and Troncoso say that they suspect that once amyloid-beta clumps start forming, those deposits collect whatever protein is available, leaving little or none to circulate in the blood.