Accumulations of amyloid β (Aβ) in the brain contribute to the development of Alzheimer’s disease, so scientists have long puzzled over why the body produces this peptide. Researchers led by Rudolph E. Tanzi and Robert D. Moir, both of Massachusetts General Hospital, in Charlestown, and Harvard Medical School, believe they have solved the puzzle. They’ve found evidence that Aβ has antimicrobial activity (PLoS One 2010, 5, e9505). “For years, we thought that Aβ was just metabolic garbage produced as a by-product of other processes within the brain,” Tanzi says. But “these data suggest it is a normal component of the brain’s innate immune system,” which protects the body from a wide range of pathogens, he explains. “It looks like factors that trigger hyperactivity of the innate immune system—not only infection but also traumatic brain injury and stroke, which are already known to increase the risk for Alzheimer’s—could cause excessive deposition of Aβ.” This hypothesis “stands in stark contrast to current models of Aβ-mediated pathology,” the researchers note, and has important implications for treatment strategies for Alzheimer’s disease.