Clearing out Alzheimer’s plaques

Alzheimer’s disease (AD) patients tend to have elevated levels of TGF-ß, or transforming growth factor beta, an immune system molecule that plays a key role in activating immune response to injury.

A multi-center group of researchers has found that blocking TGF-ß pathways in mice genetically engineered to display symptoms of AD clears the amyloid plaques in the brain that are a hallmark of the disease. Mice with tamped-down TGF-ß also show minor improvements navigating certain mazes.

In the June issue of Nature Medicine, a team led by Terrence C. Town, Ph.D., of Cedars-Sinai Medical Center in Los Angeles, and Richard A. Flavell, Ph.D., chair and Sterling Professor of Immunobiology and Howard Hughes Medical Institute investigator, reports that interrupting TGF-ß pathways in the mice allowed immune cells to engulf and digest about 90 percent of the plaques in their brains. “It was like a vacuum cleaner had removed the plaques,” says Flavell.

Town, the study’s lead author, says that if these results are supported by studies in humans, “we may be able to develop a drug that could be introduced into the bloodstream to cause peripheral immune cells to target the amyloid plaques.”