[Max's Chosen Excerpts]: "The single biggest risk factor for the vast majority of chronic diseases is old age. For many diseases, in fact, a person's birth date is a larger red flag than all other known risk factors combined. But for too long, physicians thought that the aging process was impossible to modify or slow down. Like death and taxes, growing old—and the medical problems that come with it—was considered inevitable. That's starting to change. In this special news focus on aging, Nature Medicine looks at the progress being made in drug interventions for the elderly and the hurdles that remain in the pursuit of a pharmaceutical elixir for healthy aging.....Life is short—especially for children with Hutchinson-Gilford progeria syndrome, a rare disease in which individuals rapidly develop symptoms of old age, such as hair loss, wrinkled skin, arthritis and cardiovascular weakness. Affected patients typically die by the time they enter their teens. Medications exist that can ease symptoms, but there are currently no drug treatments approved specifically for this disease. So, there was excitement when a team led by Leslie Gordon, a pediatrician at Brown University's Warren Alpert Medical School in Providence, Rhode Island, reported that an experimental drug called lonafarnib—first developed for treating cancer in 1990s but later abandoned after it failed in that setting—might buy some time for children with progeria. “We learned for the first time that progeria can be improved,” says Gordon, who cofounded the Progeria Research Foundation in 1999 after her son Sam was born with the disease. In a two-year, open-label trial involving 25 affected children, lonafarnib offered slight but statistically significant improvements in bone density, vascular stiffness and other disease symptoms1. The findings, published last year, have since buoyed the small but active progeria community. And the results have potentially wider implications for researchers studying the much larger field of 'normal' aging in the elderly, too. 'With the discovery of the genetic defect [behind progeria] and the opportunity to understand exactly what goes on, it has now become quite clear at the molecular level that this is an interesting model of aging,' Francis Collins, director of the US National Institutes of Health (NIH) in Bethesda, Maryland, told Nature Medicine. Ten years ago, Collins led the team that first demonstrated the cause of progeria: mutations in the gene encoding lamin A, an important structural component in the membrane that lines the cell nucleus2....."