View larger image | Though amyloid-beta has long been implicated in Alzheimer’s disease, figuring out just how the protein harms the brain has proved tricky. A-beta appears to cause problems when it aggregates into other forms and accumulates, perhaps because of overproduction or slow clearance. In its small oligomer form, A-beta can damage synapses, message-relaying connections between nerve cells. By setting off cascades of reactions, oligomers can also damage neural extensions called dendrites. Oligomers can clump into fibrils, which then form the large amyloid plaques characteristic of the disease. Many other potential culprits are also being investigated, some of which alter A-beta activity and some of which appear to cause damage in different ways. Credit: Nicolle Rager Fuller