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.



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