Alzheimer's disease causes misfolding and aggregation of a protein fragment known as amyloid beta and its deposition as plaques in the brain. This process triggers a cascade of event that leads to neurodegeneration. A new study has found that the deadly transformation of amyloid beta into neurotoxic aggregates can be prevented through its interaction with a variant form of the amyloid beta itself. This opens up new prospects for therapies for the disease.