A chemical that is found in fruits and vegetables, such as strawberries and cucumbers, halts memory loss that accompanies Alzheimer’s disease in mice, scientists have found.
Researchers at the Salk Institute for Biological Studies in the US found that in mice that normally develop Alzheimer’s symptoms less than a year after birth, a daily dose of the compound – a flavonol called fisetin – prevented the progressive memory and learning impairments.
The drug, however, did not alter the formation of amyloid plaques in the brain, accumulations of proteins which are commonly blamed for Alzheimer’s disease.
The new finding suggests a way to treat Alzheimer’s symptoms independently of targeting amyloid plaques, researchers said.
“We had already shown that in normal animals, fisetin can improve memory,” said Pamela Maher, senior staff scientist in Salk’s Cellular Neurobiology Laboratory who led the new study.
“What we showed here is that it also can have an effect on animals prone to Alzheimer’s,” Maher said.
More than a decade ago, Maher discovered that fisetin helps protect neurons in the brain from the effects of ageing.
She and her colleagues have since – in both isolated cell cultures and mouse studies – probed how the compound has both antioxidant and anti-inflammatory effects on cells in the brain.
Most recently, they found that fisetin turns on a cellular pathway known to be involved in memory.
So Maher and colleagues turned to a strain of mice that have mutations in two genes linked to Alzheimer’s disease.
The researchers took a subset of these mice and, when they were only three months old, began adding fisetin to their food. As the mice aged, the researchers tested their memory and learning skills with water mazes.
By nine months of age, mice that had not received fisetin began performing more poorly in the mazes. Mice that had gotten a daily dose of the compound, however, performed as well as normal mice, at both nine months and a year old.
“Even as the disease would have been progressing, the fisetin was able to continue preventing symptoms,” Maher said.
In collaboration with scientists at the University of California, San Diego, Maher’s team next tested the levels of different molecules in the brains of mice that had received doses of fisetin and those that had not.
In mice with Alzheimer’s symptoms, they found, pathways involved in cellular inflammation were turned on. In the animals that had taken fisetin, those pathways were dampened and anti-inflammatory molecules were present instead.
One protein in particular – known as p35 – was blocked from being cleaved into a shorter version when fisetin was taken. The shortened version of p35 is known to turn on and off many other molecular pathways.
The results were published in the journal Aging Cell.
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