Alzheimer’s disease is one of the biggest medical challenges of our time. About 30 million people worldwide are living with Alzheimer’s disease, and the numbers are predicted to increase to 100 million by 2050 if we do not find effective prevention or treatment strategies (1). Substantial evidence suggests that leading a healthy lifestyle, including regular exercise, may lower the risk of developing Alzheimer’s disease. However, the mechanisms through which exercise protects the brain and whether we could bottle these as a treatment remain controversial. On page 991 of this issue, Choi et al. (2) reveal that in a mouse model of Alzheimer’s disease, exercise improves memory through a combination of encouraging neurogenesis in the hippocampus and increasing the levels of brain-derived neurotrophic factor (BDNF), a growth factor that supports neuronal survival. Their findings suggest that agents that promote both BDNF signaling and neurogenesis might be effective in preventing or treating Alzheimer’s disease.
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