Latest Alzheimer's News
FRIDAY, May 9 (HealthDay News) — Flavonoids, compounds found in many fruits and vegetables, may be able to battle the ravages of Alzheimer's disease, a new study suggests.
In experiments with mice, two flavonoids called luteolin and diosmin reduced levels of beta-amyloid, which forms the harmful plaques that build up in the brains of those with Alzheimer's disease.
"Our lab has been investigating beta-amyloid, which is associated with Alzheimer's, and how we can reduce it using natural compounds," said lead researcher Kavon Rezai-Zadeh, from the Rashid Laboratory for Developmental Neurobiology at Silver Child Development Center at the University of South Florida.
The research team would like to use the two flavonoids to see if they can reduce amyloid plaque in humans, since they believe flavonoids would be safe and have few side effects compared with drugs that are being developed to reduce amyloid plaque.
Rezai-Zadeh also thinks that flavonoids, which have strong antioxidant properties, might guard against Alzheimer's. "A lot of these compounds can be derived from the diet, and they may have preventive effects against Alzheimer's disease," he said. "Increasing the flavonoids in your diet may help reduce the risk of Alzheimer's."
"The question is, can we use these flavonoids in people that have cognitive impairment?" Rezai-Zadeh said. "That's the million-dollar question."
The report was published in the May 8 online edition of the Journal of Cellular and Molecular Medicine.
In the study, Rezai-Zadeh's team used a mouse model of Alzheimer's disease to test their theory. Using, luteolin and diosmin, the researchers were able to reduce the levels of beta-amyloid in the rodents' brains.
In addition, the researchers found these two molecules were targeting a protein called presenilin-1, which has been linked to a genetic cause of Alzheimer's disease. These findings could lead to a new approach for treating Alzheimer's patients, they said.
One expert is concerned this potential treatment could also affect a patient's cognitive functioning.
"The authors of this study believe that they have identified a drug with a reasonable safety record that could reduce both plaques and tangles," said Greg M. Cole, associate director of the Alzheimer's Disease Research Center at the UCLA David Geffen School of Medicine in Los Angeles.
However, the enzyme (GSK3) targeted by these flavonoids has many important functions, including a role in processes required for normal cognitive function, Cole said.
"In fact, complete inhibition of GSK3 causes neurons to degenerate. Since cognitive function was not evaluated in this study, researchers still need to learn how much inhibiting GSK3 will be beneficial and side effect-free. That said, this may be a promising new direction," Cole said.
Another expert cautions that promising findings in mice often do not translate into effective treatments in humans.
"While this paper also shows some promising results in amyloid-depositing mice, we know from our recent experience with Alzhemed [a drug to treat Alzheimer's] and statins that the path from 'mouse cures' to 'human cures' may be a tough path indeed," said Dr. Sam Gandy, chairman of the National Medical and Scientific Advisory Council at the Alzheimer's Association and associate director of the Mount Sinai Alzheimer's Disease Research Center at Mount Sinai School of Medicine in New York City.
"Both Alzhemed and statins were effective in mice, yet failed in the clinic, so the flavonoid data join NSAIDs, vaccines, PBT2, IVIg, secretase modulators, among others, in the queue of interventions that look promising in mice but remain to be thoroughly assessed in humans," Gandy said.
SOURCES: Kavon Rezai-Zadeh, Ph.D., Rashid Laboratory for Developmental Neurobiology at Silver Child Development Center, University of South Florida, Tampa; Sam Gandy, M.D., Ph.D., chairman, National Medical and Scientific Advisory Council, Alzheimer's Association, Mount Sinai Professor of Alzheimer's Research, associate director, Mount Sinai Alzheimer's Disease Research Center, Mount Sinai School of Medicine, New York City; Greg M. Cole, Ph.D., neuroscientist, Greater Los Angeles VA Healthcare System, and associate director, Alzheimer's Disease Research Center, UCLA David Geffen School of Medicine; May 8, 2008, Journal of Cellular and Molecular Medicine, online
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