It's like the molecular version(分子的版本) of the Joker and the Riddler teaming up against Batman. Scientists at Yale University have discovered that amyloid(澱粉質的 amyl-oid)-beta, a protein involved in Alzheimer's disease(阿滋海默症;老年痴呆症), can damage brain cells by binding to prion proteins, which are themselves infamous(聲名狼藉的) because, in their abnormal form, they cause things like mad cow disease(狂牛症).
Amyloid beta is best known as the protein that forms the giant plaques(血小板) that riddle the brains of people with Alzheimer's. Those plaques contain billions of copies of amyloid beta all stuck together in one gloppy (黏糊狀液體的 glop-y) 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(重傷罪) 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(斜面 這邊當動詞用) 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.