A natural compound found in strawberries and other fruits and vegetables could help to prevent Alzheimer’s disease and other age-related neurodegenerative diseases, new research suggests.
Researchers from the Salk Institute for Biological Studies in La Jolla, CA, and colleagues found that treating mouse models of aging with fisetin led to a reduction in cognitive decline and brain inflammation.
Senior study author Pamela Maher, of the Cellular Neurobiology Laboratory at Salk, and colleagues recently reported their findings in The Journals of Gerontology Series A.
Fisetin is a flavanol present in a variety of fruits and vegetables, including strawberries, persimmons, apples, grapes, onions, and cucumbers.
Not only does fisetin act as a coloring agent for fruits and vegetables, but studies have also indicated that the compound has antioxidant properties, meaning that it can help to limit cell damage caused by free radicals. Fisetin has also been shown to reduce inflammation.
Over the past 10 years, Maher and colleagues have conducted a number of studies showing that the antioxidant and anti-inflammatory properties of fisetin could help to protect brain cells against the effects of aging.
One such study, published in 2014, found that fisetin reduced memory loss in mouse models of Alzheimer’s disease. However, that study focused on the effects of fisetin in mice with familial Alzheimer’s, which the researchers note only accounts for up to 3 percent of all Alzheimer’s cases.
For the new study, Maher and team sought to determine whether fisetin might have benefits for sporadic Alzheimer’s disease, which is the most common form that arises with age.
To reach their findings, the researchers tested fisetin in mice that had been genetically engineered to age prematurely, resulting in a mouse model of sporadic Alzheimer’s disease.
When the prematurely aging mice were 3 months old, they were divided into two groups. One group was fed a dose of fisetin with their food every day for 7 months, until they reached the age of 10 months. The other group did not receive the compound.
The team explains that at 10 months of age, the physical and cognitive states of the mice were the equivalent to those of 2-year-old mice.
All rodents were subject to cognitive and behavioral tests throughout the study, and the researchers also assessed the mice for levels of markers linked to stress and inflammation.
The researchers found that the 10-month-old mice that did not receive fisetin showed an increase in markers associated with stress and inflammation, and they also performed significantly worse in cognitive tests than mice that were treated with fisetin.
“At 10 months, the differences between these two groups were striking,” notes Maher.
In the brains of the non-treated mice, the researchers found that two types of neurons that are usually anti-inflammatory – astrocytes and microglia – were actually promoting inflammation. However, this was not the case for the 10-month-old mice treated with fisetin.
What is more, the researchers found that the behavior and cognitive function of the treated mice were comparable with those of 3-month-old untreated mice.
The researchers believe that their findings indicate that fisetin may lead to a new preventive strategy for Alzheimer’s, as well as other age-related neurodegenerative diseases.
“Based on our ongoing work, we think fisetin might be helpful as a preventative for many age-associated neurodegenerative diseases, not just Alzheimer’s, and we’d like to encourage more rigorous study of it,” says Maher.
However, the researchers note that human clinical trials are required to confirm their results. They hope to team up with other investigators to meet this need.
“Mice are not people, of course. But there are enough similarities that we think fisetin warrants a closer look, not only for potentially treating sporadic AD [Alzheimer’s disease] but also for reducing some of the cognitive effects associated with aging, generally.”