Two research groups have independently published findings related to Alzheimer's disease treatments. Both experimental therapies target amyloid β, the protein believed to cause the disease. Weihong Song of the University of British Columbia, Vancouver, and colleagues treated mice with valproic acid, a compound already used as an anticonvulsant and mood stabilizer for patients with epilepsy, bipolar disorder, and other conditions. They found that valproic acid reduced enzymatic production of amyloid β by γ-secretase. The treatment prevented brain cell death and axon damage and improved memory in mice that were in early stages of Alzheimer's (J. Exp. Med., DOI: 10.1084/jem.20081588). Li Gan of the University of California, San Francisco, and coworkers took another approach. Instead of limiting the formation of amyloid β, they opted to increase its degradation in mice. The researchers boosted the activity of cathepsin B—an enzyme that breaks down amyloid β—by reducing levels of cystatin C, an enzyme that inhibits cathepsin B activity. The mice in the experiment showed improvements in learning and memory (Neuron 2008, 60, 247).