Researchers may have pinpointed the cause of Alzheimer’s disease: a rogue protein called amyloid beta that forms plaques in the brain.

Drugs that reduce this protein in humans may have the same protective effect.

In experiements with a strain of Alzheimer’s disease-prone mouse, as the animals age, amyloid beta levels rise and their memory declines. But when a key enzyme, called BACE1, is eliminated through genetic engineering, the mice stay dementia-free. This enzyme helps to make amyloid beta. Without it, the protein levels stay low and nerve cells stay healthy.