A study by the Salk Institute for Biological Studies found that a daily serving of fisetin, an antioxidant commonly found in fruits and vegetables, reduced Alzheimer’s symptoms in mice who were predisposed to the disease. Previous studies on fisetin have revealed this flavonoid’s positive effect on the degenerative aging of brain neurons.
The drug did however not stop amyloid plaques from forming in the brain. These are typically blamed for Alzheimer’s disease, and the new results suggest a way to treat Alzheimer’s separately from targeting amyloid plaques. It may also indicate that Fisetin helps in combating Alzheimer’s but not cure it.
“We had already shown that in normal animals, fisetin can improve memory,” Pamela Maher, leader of the study and senior staff scientist in Salk’s Cellular Neurobiology Laboratory said in a statement. “What we showed here is that it also can have an effect on animals prone to Alzheimer’s.”
Maher and her colleagues from the Salk Institute began adding fisetin to food for 3-month-old mice who had two gene mutations linked to Alzheimer’s. Throughout the course of six months, each mouse had their memory and learning skills tested through a series of water maze tests. At 9 months of age, mice that were fed a daily dose of fisetin performed remarkably well on these tests compared with mice that did not receive any of the flavonoid.
Further research performed in collaboration with the University of California, San Diego compared different molecules in the brains of both the mice that did not receive fisetin and those that did. Mice affected by Alzheimer’s had pathways of cellular inflammation that were turned on, but these same pathways were replaced by dampened and anti-inflammatory molecules in mice that were not experiencing any trouble with learning and memory.
“What we realized is that fisetin has a number of properties that we thought might be beneficial when it comes to Alzheimer’s,” Maher explained. “Even as the disease would have been progressing, the fisetin was able to continue preventing symptoms. It seems to act on other pathways that haven’t been seriously investigated in the past as therapeutic targets.”