Professor Dennis Selkoe explains that amyloid beta oligomers - small assemblies of amyloid beta protein associated with Alzheimer's disease - do not cause plaques but prevent them.

Amyloid beta oligomers are small assemblies or aggregates of this so-called amyloid beta protein, which I’ll call a-beta. We discovered in 1992, that everyone makes a-beta, or amyloid beta, in a singlet form. We use the term monomer for that. It’s just one copy, and the cell spews out one copy and then it spews out another. And we discovered that, rather than amyloid beta just being involved with Alzheimer’s [disease], it’s involved in all of us – it’s made normally. The analogy is cholesterol and hardening of the arteries or heart disease. Everyone makes cholesterol; if it builds up in the wrong places, you can get a heart attack. The story turns out to be similar in Alzheimer’s disease; a-beta is made by everyone, but it is made almost exclusively as a single form, and if you make too much a-beta, and there are inherited reasons why a person might, then one monomer or singlet will find another monomer or singlet and team up and make a doublet. And so, when I use the term dimer, it is synonymous with calling it a doublet. And then, if another one joins to a doublet, you have a triplet, or a trimer. And if you have another one you have a quadruplet, or a tetramer. So, this process of adding a-beta molecule by molecule to another a-beta is called oligomer formation. 'Oligo' means few, a few 'mers.' 'Mer' means a single unit. So, we think that oligomers of a-beta are the smoking gun in Alzheimer’s [disease]. We think they are able (because they are small) to diffuse into the synapse, the space between two nerve cells which transmits information; there they can cause trouble. Now, people have known for a long time that amyloid beta protein forms huge plaques in the brain. They are not really huge because you still have to use a microscope to see them, but they are much bigger than doublets, or triplets, or quadruplets. They probably have a million a-beta molecules or more in a plaque. We’ve come to the conclusion from our research over the last few years, and other scientists agree with this, that the plaques themselves are a reservoir of lots and lots of a-beta molecules and these reservoirs themselves are not directly toxic. If anything, we’ve started to come to the conclusion that they are protective, and the simple analogy would be a jail, if you will. So, if you have quite a lot of bad guys in the society, if you put them in jail, at least during the time they are in jail they are not causing trouble at that moment. But, it’s a problem for society if there are a lot of jails with a lot of bad guys going into them, and the plaques are a problem for Alzheimer’s [disease] patients. While I say the plaques are protective, at the same time some a-beta doublets and triples come off the plaque. There is a so called off-rate, and there is an on-rate, the rate by which new doublets and triplets get into the plaque. The plaque is dynamic, and that’s bad news if you wish. If everything stayed locked up in a plaque, perhaps patients wouldn’t have symptoms. But because the plaques have a limit on what they can hold, the jails become full and other people – other a-beta molecules – are out there wreaking havoc.

amyloid beta protein, oligomer, alzheimer, dimer, plaque, dennis, selkoe