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

It’s like the molecular¹ version of the Joker and the Riddler³ 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 binding⁴ to prion proteins, which are themselves infamous⁵ because, in their abnormal form, they cause things like mad cow disease.

Amyloid beta is best known as the protein that forms the giant plaques⁶ that riddle² 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 soluble⁷ 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, impairing⁸ their ability to learn. And the Yale researchers wanted to find out how.

They discovered that amyloid beta binds⁹ to the prion proteins normally found on neurons. What’s more, the prions ramp¹⁰ 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 potent¹¹ weapon against Alzheimer’s.

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