A Compound in Strawberries can Arrest Memory Loss in Alzheimer’s Patients
A study suggests that a compound in strawberries may help in combating memory loss that accompanies Alzheimer's disease.
The study led by scientists at the Salk Institute for Biological Studies claims that a naturally occurring chemical compound fisetin found in many fruits and vegetables - from strawberries to cucumber- helps in arresting memory loss that occurs with Alzheimer's disease. The study was conducted on mice.
A daily dose of the antioxidant helped in preventing the progressive memory and learning impairments in mice as they aged. These effects were even noticed in the mice with genetic mutations associated with Alzheimer's. This antioxidant however did not affect the formation of the amyloid plaques in the brain. These plaques are often associated with Alzheimer's disease.
"Fisetin didn't affect the plaques. It seems to act on other pathways that haven't been seriously investigated in the past as therapeutic targets," Pamela Maher, a senior staff scientist in Salk's Cellular Neurobiology Laboratory, said in a statement.
Previously, Maher and colleagues had shown that the antioxidant fisetin helps in improving memory. The present study has shown that this antioxidant is equally effective on animals vulnerable to Alzheimer's disease.
About ten years ago, Maher had discovered that the flavanol fisetin protected the neurons in the brain from the effects of aging. Since then, researchers have tried to find how the compound has both antioxidant and anti-inflammatory effects. They have discovered that the flavanol activates a cellular pathway linked with memory.
In the current study, the researchers worked on a strain of mice that had two mutated genes linked with Alzheimer's. A subset of these mice was given fisetin along with their food since they were three months old. As these mice aged, the researchers tested the memory and learning skills with water maze experiments.
The researchers noticed that those mice that were not given fisetin performed poorly on the maze whereas the mice that had fisetin since three months of age performed as good as normal mice.
"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."
It was also seen that when the mice were fed fisetin, a particular protein p35 was blocked from splitting into a shorter version. The shorter version of the protein activates and blocks several molecular pathways.
"The model that we used here was a preventive model," explains Maher. "We started the mice on the drugs before they had any memory loss. But obviously human patients don't go to the doctor until they are already having memory problems." So the next step in moving the discovery toward the clinic, she says, is to test whether fisetin can reverse declines in memory once they have already appeared.
The study is documented in the journal Aging Cell.
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