SSS 2009-03-02（在线收听）

This is Scientific American's 60-Second Science. I'm Karen Hopkin. This will just take a minute.

It’s like the molecular version of the Joker and the Riddler teaming up against Batman. Scientists at Yale University have discovered that amyloid beta, a protein involved in Alzheimer’s disease, can damage brain cells by binding to prion proteins, which are themselves infamous because, in their abnormal form, they cause things like mad cow disease.

Amyloid beta is best known as the protein that forms the giant plaques that riddle the brains of people with Alzheimer’s. Those plaques contain billions of copies of amyloid beta all stuck together in one gloppy mess. But the protein also exists in a more soluble form, either in single units or in small groups of 50 or 100. These smaller clusters don’t cause the same large-scale mayhem as plaques, but they do damage neurons, impairing their ability to learn. And the Yale researchers wanted to find out how.

They discovered that amyloid beta binds to the prion proteins normally found on neurons. What’s more, the prions ramp up amyloid beta’s neurotoxic effects. Take away the prions and amyloid-beta clusters are harmless, findings published in the journal Nature. So drugs that prevent this amyloid–prion coupling could be a potent weapon against Alzheimer’s.

Thanks for the minute for Scientific American's 60-Second Science. I'm Karen Hopkin.