NEW YORK (Reuters Health) – Protein accumulations, or plaques, characteristic of Alzheimer's disease can be eliminated from the brains of mice, researchers report, by encouraging scavenger immune cells called macrophages to do their work.

The activity of macrophages is damped down by a naturally occurring compound called TGF-beta, to stop runaway reactions, and prior research has shown that brain levels of TGF-beta are increased in patients with Alzheimer's disease, according to the report in the research journal Nature Medicine.

Some researchers believed that the high levels of TGF-beta were simply an attempt to quiet the inflammatory response associated with Alzheimer plaques. However, the new findings contradict that notion.

The researchers genetically engineered mice to block TGF-beta signaling in macrophages in the peripheral circulation. They found that this "promotes the influx of these cells into brains of Alzheimer's mice," lead author Dr. Terrence Town, from Yale University School of Medicine in New Haven, Connecticut, told Reuters Health.