Posted on Jul 19, 2017, 8 a.m.
Researchers find further evidence that strawberry nutrients may reduce the mental effects of aging.
Salk scientists have uncovered evidence that a natural compound found in strawberries decreases the mental effects of the aging process. The specific compound in question is the antioxidant fisetin. The scientists used a mouse model to replicate premature aging in human beings including Alzheimer's disease. This recent finding builds upon previous evidence that indicated natural compounds in strawberries minimize cognitive deficits as well as inflammation. The findings were recently published in an issue of Journals of Gerontology Series A. The hope is that strawberries' antioxidant fisetin will help treat mental decline stemming from the aging process and conditions such as Alzheimer's and strokes.
Companies have used fisetin in a wide array of health products across the past couple of decades. However, there has not been a considerable number of tests to gauge the legitimacy of this compound in relation to improving health. Salk Cellular Neurobiology Laboratory staff scientist Pamela Maher served as the senior author of the above-referenced study. She states that based on her team's current work, there is an expectation that fisetin might prove helpful at preventing all sorts of age-related neurodegenerative diseases. She is adamant that the scientific community should perform a rigorous study of this antioxidant.
Maher also works in David Schubert's lab. Schuber is the head of the Salk Cellular Neurobiology lab. He has been studying fisetin across an entire decade. Prior research by this lab determined fisetin decreases memory loss linked to Alzheimer's in mice that were genetically altered to develop this crippling disease. However, this study keyed in on genetic AD that accounts for about two percent of cases.
The larger risk factor for developing sporadic AD and a number of other neurodegenerative disorders is age. Maher used a strain of lab mice that prematurely aged to gain a better understanding of sporadic AD. When these mice reached an age of 10 months, they usually displayed signs of cognitive as well as physical decline not observed in regular mice until they reached two years of age.
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The Salk scientists fed three-month-old prematurely aging mice a dose of fisetin each day. This dose was provided across a seven-month span. A separate group of prematurely aging mice was provided with the same food yet fisetin was not included. During this study period, the mice were subjected to memory and activity tests. The scientists studied levels of proteins in mice related to brain function, inflammation, and responses to stress.
When the mice in the study reached 10 months, the differences between the two groups proved eye-opening to say the least. Mice that were not provided with fisetin endured difficulties with the cognitive tests. They also displayed elevated stress markers and higher levels of inflammation. The brain cells known as microglia and astrocytes that are typically anti-inflammatory spurred excessive inflammation.
Alternatively, mice provided with fisetin did not display major differences in cognitive ability, inflammatory or behavior markers at the 10-month mark when compared to a group of three-month-old mice with the same condition who were untreated. Furthermore, there was no evidence that acute toxicity existed in mice treated with fisetin. This was also true for mice provided with high doses of fisetin.
Though mice are not exactly the same as human beings, the Salk scientists believe fisetin deserves a closer look. It might prove quite effective in treating sporadic AD in humans and also decreasing cognitive effects tied to the aging process. Maher is looking to team up with another group to complete fisetin clinical trials with human beings.
Antonio Currais, Catherine Farrokhi, Richard Dargusch, Aaron Armando, Oswald Quehenberger, David Schubert, Pamela Maher. Fisetin Reduces the Impact of Aging on Behavior and Physiology in the Rapidly Aging SAMP8 Mouse. The Journals of Gerontology: Series A, 2017; DOI: 10.1093/gerona/glx104