Alzheimer's disease represents the most common form of dementia, with the early stages of the disease generally characterized with short term memory loss and learning difficulties that increase in severity as the patient progresses in age. Scientists at the Salk Institute for Biological Studies, California, have discovered that with regular treatments of the antioxidant fisetin, they were able to prevent memory loss in mice with genetic mutations linked to Alzheimer's.

Whilst the cause and progression of Alzheimer's are not well understood, current theories link the existence of the disease to amyloid plaques and tangles in the brain. There is currently no cure or treatment to either eradicate or halt the advance of the disease, however the research carried out by the Salk Institute for Biological Studies is a good example of how scientists are instead attempting to combat the symptoms of the debilitating disease.

It was found that fisetin, a chemical commonly found in fruits and vegetables such as strawberries, apples and grapes, prevents loss of memory and reduces learning difficulties in mice as they age.

The compound was tested by administering it once a day to mice with the Alzheimer's mutation from the age of three months. The mice were then put through a water maze designed to test their short term memory and learning skills.

The tests showed that, once the mice were nine months old, those that had not been administered the fisetin began to struggle with the maze, whilst those that had been treated with fisetin performed as well as a mice who did not have the genetic mutations linked to Alzheimer's disease.

"We had already shown that in normal animals, fisetin can improve memory," said Pamela Maher, a senior staff scientist in Salk's Cellular Neurobiology Laboratory. "What we showed here is that it also can have an effect on animals prone to Alzheimer's."

The team found that the fisetin didn't affect the amyloid plaques, but that pathways involved with cellular inflammation were dampened and anti-inflammatory molecules were present. Additionally, fisetin prevented a protein known as p35 from being cleaved into a shorter version – this shorter version is known to turn many molecular pathways on and off. Examining whether fisetin affects targets other than p35 will be a focus of further research.

"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."

The scientists will also examine the effect that the timing of the administration of fisetin can have on the disease. Maher was also keen to highlight that the tests involved a preventative model, with the drugs administered to the mice before they had exhibited any memory loss. Because people don't seek treatment before they have memory problems, the next logical step in the study would be to examine whether the application of fisetin could reverse the deteriorating effects of Alzheimer's that have already taken place.

The results of the team's study were published in the journal Aging Cell.