Riddled with deposits of a peptide called beta-amyloid, the brain can become consumed with plaque, which builds up in the spaces between nerve cells. When nerve cells begin to die off, symptoms of Alzheimer’s disease set in.
Natural flavanol works beyond plaque to restore memory
In areas of the brain where memory is important, tangles of plaque can develop from twisted fibers of tau protein. Alzheimer’s, the most common form of dementia, has always been recognized by this plaque buildup, which is associated with problems in thinking, memory and behavior. As a condition that slowly worsens over time, Alzheimer’s is ultimately capable of interfering with daily tasks and newly learned information.
New findings suggest that Alzheimer’s can be reversed. A new fruit- and vegetable-based treatment could effectively bypass plaque formation and work independently to restore memory in the nerve cells of the brain, turning on specific memory-related pathways.
Nerve cells work together in vast networks
With over 100 billion nerve cells at work in the brain, communicating in vast networks, cellular protection is vital. Nerve cells specialize in some of the most complicated areas of the human experience, including jobs like smell, taste, hearing, learning, thinking,and memory. Operating like miniature factories, nerve cells perform an array of functions, including obtaining necessary supplies, communication, energy generation, information storage and waste removal. Scientists have a hard time pinpointing how Alzheimer’s takes hold in a person as they age.
See also: preventing Alzheimer’s
Fisetin improves memory of Alzheimer’s-ridden mice
How might specific properties of fruits and vegetables help stop memory loss as seen in Alzheimer’s disease?
One flavanol, fisetin, was isolated, studied and put to the test in Alzheimer’s-ridden mice. Scientists at the Salk Institute for Biological Studies have discovered that a daily dose of this fruit and vegetable compound can help mice recover their memory.
The fisetin surprised the scientists, showing promise for improving memory even as amyloid plaque formation stayed the same. These accumulations of proteins remained prevalent in Alzheimer’s mice and continued gumming up nerve cells even after fisetin was administered, but their memory improved independent of the plaque formations. This new finding suggests that there may be a way to treat Alzheimer’s symptoms without combating amyloid plaques.
“Fisetin didn’t affect the plaques,” says Maher. “It seems to act on other pathways that haven’t been seriously investigated in the past as therapeutic targets,” says Pamela Maher, a senior staff scientist in Salk’s Cellular Neurobiology Laboratory who led the new study.
Over 10 years ago, Maher learned that fisetin helped protect neurons in the brain, after isolating the flavanol in cell cultures and examining its anti-inflammatory, antioxidant prowess in nerve cells. In her research, fisetin was found to turn on a specific cellular pathway that improves memory.
Fisetin working on the molecular level
Working with Dave Schubert, leader of the Cellular Neurobiology Lab, Maher conducted her tests on a group of mice with two gene mutations linked to Alzheimer’s.
After feeding the fisetin to the mice at three months old, the researchers began studying how the natural substance affected mice in a variety of learning skills and water mazes.
At just nine months of age, mice receiving no fisetin performed more poorly in the water mazes. These Alzheimer’s-destined mice would normally show memory deficits by the first year, but after eating fisetin, they performed just as well as normal mice, at both nine months old and one year of age.
“Even as the disease would have been progressing, the fisetin was able to continue preventing symptoms,” Maher says.
To investigate further, Maher collaborated with scientists at the University of California, San Diego, to key in on specific brain molecules. What they found was that fisetin turned on pathways involved in cellular inflammation. Anti-inflammatory molecules were observed in specific areas of the brain involved in memory after pathways were triggered on.
When fisetin was administered, p35 protein was blocked from being cut down into a shorter form. Short versions of the p35 protein are responsible for turning many molecular pathways on and off.
“It may be that compounds like this that have more than one target are most effective at treating Alzheimer’s disease,” says Maher, “because it’s a complex disease where there are a lot of things going wrong.”
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