The aggregated proteins strewn about the brain are the hallmark of one of the most common neurodegenerative disorders: Alzheimer's disease. But while these irregular, gunky proteins, called amyloid-beta, are believed to contribute to the deterioration of memory and cognitive ability in Alzheimer's patients, no one knows how they lead to these symptoms. New experiments show how amyloid-beta interacts with a clotting agent in the blood, increasing blood clots that are harder than usual to break down and starving neurons of their regular supply of oxygen. The research suggests that the effects of amyloid-beta on the blood vessels feeding the brain could be an important aspect of the havoc they wreak on the brain.