There is a natural product in strawberries that slows mental decline

An article published by the American Salk Institute in the Journals of Gerontology Series A shows that there is a natural product in strawberry that not only improves the condition of hereditary Alzheimer's disease, but also reduces cognitive dysfunction and inflammation associated with aging in mice. .

Further evidence from the Salk Institute in the United States indicates that there is a natural product in strawberries that reduces cognitive dysfunction and inflammation associated with aging in mice. Related articles were recently published in the Journals of Gerontology Series A.

Fexone is a naturally occurring flavonoid. In addition to strawberries, tomatoes, onions, oranges, apples, peaches, grapes, kiwis and persimmons also contain fisetin.

Previous studies have demonstrated that fisetin improves hereditary Alzheimer's disease

The study was based on previous research by the team on fisetin, which was found to help treat age-related mental decline and Alzheimer's or stroke.

Maher, who works at the David Schubert Laboratory of Cell Neurobiology at the Salk Institute, has been studying fisone for more than a decade. Previous laboratory studies (published on Aging Cell in March 2014) found that fisetin can reduce memory loss in Alzheimer's mice constructed by genetic modification. But the study is targeted at hereditary (familial) Alzheimer's disease, which accounts for only 1 to 3% of cases.

Pamela Maher, senior author of the article, said: "Many companies have added fisetin to a variety of health foods, but there is a lack of more rigorous testing of the compound. Based on the work we do. We believe that fisetin can be used Preventing many age-related neurodegenerative diseases, not just Alzheimer's. What we do is to encourage more rigorous research on the natural products in this fruit."

Fasone can prevent cognitive decline in premature aging mice

To date, the greater risk factor for sporadic Alzheimer's disease and other neurodegenerative diseases is age. In the current survey, Maher chose a laboratory mouse strain that had premature aging to better study sporadic Alzheimer's disease. After 10 months, these mice show signs of decreased physical and cognitive abilities, which usually occur in normal mice until two years.

The Salk team added a daily dose of fisetin to the food of prematurely aged mice at 3 months for 7 months. Another group of premature aging mice were fed the same food but no fisetin. Mice were subjected to a variety of activities and memory tests during the study period. The team also studied specific protein levels in mice associated with brain function, stress response, and inflammatory response.

Maher said: "In the 10th month, the difference between the two groups is amazing." No mice treated with fisetin have difficulty in all cognitive tests, markers of stress and inflammation high. Brain cells called astrocytes and microglia are usually anti-inflammatory and are now causing inflammation. Ten-month-old mice treated with fisetin were no different in behavioral, cognitive, or inflammatory markers than untreated 3-month-old mice (without signs of aging). In addition, the team found that even with high doses of the compound, there is no evidence that fisetin is acutely toxic to treated mice.

Maher said: "Of course the mouse is not a human. But there is enough similarity with humans. We believe that fisacetone deserves careful study, not only as a potential treatment for sporadic Alzheimer's disease, but also to reduce some common, The cognitive decline associated with aging.” Next, Maher hopes to work with other research groups or companies on human clinical trials of fisetin.

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