Now more than ever, Alzheimer's disease poses an enormous burden. The neurodegenerative disease afflicts more than five million Americans, robbing them of their memories and placing strain and heartache on their loved ones. This toll costs the U.S. economy hundreds of billions of dollars each year.

But a new study of mice published in the Journal of Experimental Medicine suggests that by shutting off just one protein, future medications could potentially break up the sticky plaques associated with Alzheimer's.

The protein in question, BACE1, plays a fundamental role in neural development. It also makes the raw materials that form beta-amyloid plaques, the sticky gloms of protein found in the brains of Alzheimer's patients. Some researchers suspect that as beta-amyloid