A compound in green tea appears to slow the progression of Alzheimer’s disease in mice when combined with exercise, and may even reverse its effects.
The commonly found extract could also lead to new treatments to prevent Alzheimer’s in people, says Todd Schachtman, professor of psychological sciences at the University of Missouri:
“In Alzheimer’s patients, amyloid-beta peptide (A-beta) can accumulate and clump together causing amyloid plaques in the brain.”
Increases in inflammation have been linked to Alzheimer’s disease patients and recent studies have suggested the benefits of dietary antioxidants in reducing risk.
Based on earlier studies, researchers decided to investigate the effects of voluntary exercise and epigallocatechin-3-gallate (EGCG), a green tea extract, on memory function and A-beta levels in mice known to show plaque deposits and behavior deficits.
First, mice were placed in the center of a specialized maze and allowed to move around with the aim of finding the right hole, or “goal box.” Researchers watched the mice to determine whether or not they could find the goal box, demonstrating memory and cognition.
In the second test, small “nestlets,” or squares containing materials to create nests, were placed in the habitats for different groups of mice. A day later, nests were scored based on shape and the amount of material used.
Bad Nest Day
“Mice exhibiting symptoms of the disease had nests that were poorly formed or erratic,” Schachtman says. “Further, we found that mice with Alzheimer’s symptoms, much like people, can be apathetic about their habitat, or have forgotten how to ‘nest’ appropriately.”
Researchers then added the extract to the mice’s drinking water and gave them access to running or exercise wheels. Alzheimer-affected mice that were given EGCG and allowed to exercise showed remarkable improvements in cognitive function and retention.
Grace Sun, professor emerita of biochemistry, said:
“Oral administration of the extract, as well as voluntary exercise, improved some of the behavioral manifestations and cognitive impairments of Alzheimer’s. We also are excited to see a decrease in A-beta levels in the brains of the affected mice as well as improvements in behavior deficits in mice with AD.”