Kat Arney: Alzheimer’s is a disease that affects more than 20 million people around the world, and it’s basically a degenerative brain condition that’s currently essentially incurable. We do know that many of the effects of Alzheimer’s are due to the build-up of a protein called amyloid beta and this makes lumps called plaques in the brain, but until now it’s not really been clear exactly how the amyloid protein starts to build up in brain cells or how it really causes the illness. However, this week, scientists in the US have discovered that this build-up of amyloid might be aided by a rogue protein, the prion protein.
Chris Smith: It’s the same thing that’s been implicated in mad cow disease and BSE isn’t it?
Kat: Absolutely, yes. This prion protein called PrP is normally found in many different cells and it sits in the cell membrane, and normally it does a useful job, for example in the brain it helps brain cells to respond to changes in the environment around them, but sometimes the prion protein is found in a different shape, a different conformation, and this is where the trouble really starts.
Chris: How does Alzheimer’s come into it?
Kat: Well, writing in this week’s edition of the journal Nature, the researchers discovered that amyloid beta can stick to the normal form of the prion protein and this might be what’s causing amyloid to build up in brain cells. Importantly, they discovered that little groups of amyloid are more likely to stick to the prion protein than single amyloid molecules, suggesting that this really is a key for building up amyloid plaques.
Chris: But does this actually have an effect on the function of the brain? How can we actually be sure it’s really important for the development of the disease itself?
Kat: Well the scientists then went on to look at samples of mouse brains. They were particularly looking at the hippocampus, this is the part of the brain that’s involved in your learning and your memory and it’s badly affected in Alzheimer’s, and they found that brain samples from normal mice, they found the build-up of amyloid protein blocked a process called long-term potentiation, which is basically how the brain builds memories. But in samples from mice that lacked the prion protein, amyloid didn’t cause these problems with long-term potentiation, so this really does show that the prion protein’s a key link in the chain.
Chris Smith: And what are they going to do next about this?
Kat: Well this discovery is pretty exciting because it gives us a whole new angle for new Alzheimer’s treatments. Perhaps if researchers could develop drugs that block the interaction between amyloid and the prion protein, then this might be a good way to prevent the plaques building up.