Aerobic exercise has been shown to improve cognitive function in neurodegenerative diseases, such as Alzheimer’s, and recovery following peripheral nerve injuries in animals. A previous report found that daily running may significantly reduce the risk of age-related macular degeneration by as much as 10%.

Following up with these studies, researchers recently hypothesized that brain-derived neurotrophic factor (BDNF) may act as a signaling molecule to mediate the beneficial effects of exercise. Increased levels of BDNF are present in the brain, retina and skeletal muscle. Blocking this protein could eliminate the protective effects of exercise. The team’s rat model confirmed this thinking.

The researchers had one group of rats exercise on a treadmill for 30 minutes, five days a week, and placed another group on a static treadmill. After three weeks, the rats underwent optic nerve transection, which is frequently used to study neuronal degeneration-associated events in adult human central nervous systems. “In the adult rat retina, approximately 90% of retinal ganglion cells (RGCs) are lost two weeks after optic nerve transection,” the researchers noted.

After the surgery, the rats exercised for another week. Inactive rats had RGC survival rates of 67% and 39% after five and seven days, respectively. Active rats, however, did significantly better, with 74% and 48% survival rates at the same intervals. They also had significantly higher BDNF levels in response to exercise.

The data suggests BDNF levels may be related to both intensity and duration of exercise. “It’s important to identify the optimal training paradigms required to increase growth factors involved in protective effects in the retina in the future,” the investigators said.

Although BDNF has a significant protective effect on RGCs, the study authors noted that therapeutic use of the protein in central nervous system diseases is limited because it doesn’t cross the blood-brain barrier. Intravitreal injections increase adult RGC survival, but the protein has a short half-life of only three hours in neuronal tissues. They concluded that aerobic exercise is a simple, low-cost lifestyle change that can chronically increase BDNF in humans.