Researchers have found that beta-amyloid-induced destruction of synapses — connections that mediate communication between nerve cells — is driven by a chemical modification to the enzyme Cdk5. This altered form of Cdk5 (SNO-Cdk5) was prevalent in human Alzheimer’s disease brains, but not in normal brains, suggesting that SNO-Cdk5 could be targeted for the development of new Alzheimer’s disease therapies.