In that aging is the single greatest risk factor for Alzheimer's Disease, Andrew Dillin, from the Salk Institute for Biological Studies (California, USA), and colleagues found that simply slowing the aging process in mice prone to develop Alzheimer's prevented their brains from succumbing to the disease.  Explaining that: "In this study, we went directly to the root cause of Alzheimer's disease and asked whether we could influence the onset of the disease by modulating the aging process," the team slowed the aging process in a mouse model for Alzheimer's by lowering the activity of the IGF-1 signaling pathway. "This highly conserved pathway plays a crucial role in the regulation of lifespan and youthfulness across many species, including worms, flies, and mice and is linked to extreme longevity in humans," he explains. As a result, mice with reduced IGF-1 signaling live up to 35 percent longer than normal mice. The team then employed a battery of behavioral tests to find out whether it was simply the passage of time or aging per se that determined the onset of the disease. Chronologically old but biologically young animals appeared nearly normal long after age-matched, normal-aging Alzheimer's mice exhibited severe impairments in tests of cognition and memory.