Alzheimer's Research Target May Be a Dead End

"To find things that will competitively stick and stop them from assembling is theoretically hard to imagine," Lynn said. It was thought that individual molecules of amyloid inhibitors might do so, but the new finding -- that the molecules inevitably bind together in a more impractical mass -- renders them therapeutically useless.

But other avenues of Alzheimer's research remain promising, Lynn said.

"There are certainly other strategies that have potential," he noted, including antibody-focused strategies aimed at eliminating plaques, or treatments focused on easing the downstream effects of amyloid buildup.

Both scientists stressed that it's still not certain whether protein plaques even cause Alzheimer's and other brain diseases, or whether they are merely byproducts of the disease process. "That's really another open area of research," Shoichet said.

"The problem with these diseases is that it is such a moving target," Lynn said. "And so, different people are looking at different things."

More information

There's much more on Alzheimer's disease at the Alzheimer's Association.

SOURCES: Brian Shoichet, Ph.D., professor, pharmaceutical chemistry, University of California, San Francisco; David Lynn, Ph.D., Howard Hughes Institute investigator and professor, biological chemistry, Emory University, Atlanta; Jan. 27, 2008,Nature Chemical Biology, online