Frustrated by repeated failures of experimental therapies that try to attack Alzheimer's by targeting the build-up of beta amyloid in the brain, researchers are going back to the drawing board to come up with a better cause for the disease--and a whole new approach to developing drugs for it.
Karl Herrup, chairman of the department of cell biology and neuroscience at Rutgers University, says he now believes that Alzheimer's is the result of a multi-step process starting with an injury to the brain--perhaps in youth or later in life after a series of small strokes--which triggers runaway inflammation.
"It allows that amyloid deposit is a risk factor. But, in my mind, it recalibrates the emphasis on amyloid and other aspects of the disease," Herrup tells the Los Angeles Times.
However, the New York Times notes that beta amyloid may well be the problem. The brain continues to manufacture beta amyloid the same as it ever did, say some researchers, but the system for disposing it has gone awry, leading to the buildup of toxic levels. Others want to try and mount a special defense of the hippocampus, the brain's memory system that is trashed by the disease.
Meanwhile, now that physicians have new tools to diagnose Alzheimer's early on, some worry that the absence of any effective treatments for the disease leaves them in a quandary over telling their patients the bad news.
- read the LA Times story on Herrup's ideas
- see the New York Times piece on the amyloid projects
- and here's the UPI report on the ethical dilemma