Salk study shows strawberries may help those with Alzheimer's disease

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Strawberries are similar to blueberries and red wine in having multiple health benefits, thanks to a compound called fisetin, the Salk Institute for Biological Studies reported recently.

Fisetin helps combat juvenile diabetes and protects neurons in the brain, according to a study by Salk researchers David Schubert, Ph.D., and Pam Maher, Ph.D., appearing in the journal, PLoS ONE.

Strawberries are the best source of fisetin, which appear to a lesser extent in other fruits and vegetables, according Maher.

Salk Institute Strawberry Study
The researchers gave Akita mice, which are afflicted with unusually high blood sugar, a fisetin-high enriched diet, and the medical effects of diabetes were eased, according to the study. There is also evidence that fisetin can protect neurons and could help slow or prevent neurological disorders such as Alzheimer's disease and Huntington's Disease, Maher said.
It would take 37 strawberries daily to equal the dosage given to the lab mice, so researchers envision fisetin not as a dietary change, but as a supplement that would be taken in pill form. Although dietary supplements containing fisetin are available in the U.S., the dose is generally lower than the equivalent dose given to the mice in the study, Maher said.

Maher said the Salk researchers have had preliminary discussion with pharmaceutical companies about fisetin. Their also plan to see if fisetin is effective in treating type 2 diabetes.

Another promising finding in the fight against Alzheimer's

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Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

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Scientists have discovered a new target for the prevention of adverse immune responses, which have been identified as factors in the development of Alzheimer's disease (AD).

The discovery was made by researchers at the University of South Florida's Department of Psychiatry and the Center of Excellence for Aging and Brain Repair.

The CD45 molecule is a receptor on the surface of the brain's microglia cells, cells that support the brain's neurons and also participate in brain immune responses.

Previous studies by the USF researchers showed that triggering CD45 was beneficial because it blocked a very early step in the development of Alzheimer's disease. In the present study, the researchers demonstrated in Alzheimer's mouse models that a loss of CD45 led to dramatically increased microglial inflammation.

Although the brain's immune response is involved in Alzheimer's disease pathology, "this finding suggests that CD45 on brain immune cells appears critically involved in dampening harmful inflammation," said study senior author Jun Tan, a professor of psychiatry and Robert A. Silver chair at the Rashid Laboratory for Developmental Neurobiology, USF Silver Child Development Center and research biologist for Research and Development Service at the James A. Haley Veteran's Hospital.

The investigators also found an increase in harmful neurotoxins, such as A beta peptides, as well as neuron loss in the brains of the test mice.

"In short, CD45 deficiency leads to increased accumulation of neurotoxic A beta in the brains of old Alzheimer's mice, demonstrating the involvement of CD45 in clearing those toxins and protecting neurons," Dr. Tan said. "These findings are quite significant, because many in the field have long considered CD45 to be an indicator of harmful inflammation. So, researchers assumed that CD45 was part of the problem, not a potential protective factor."

The next step is to apply these findings to develop new Alzheimer's disease treatments, said Paula Bickford, PhD, a professor in the USF Department of Neurosurgery and senior career research scientist at the James A. Haley Veteran's Hospital.

"We are already working with Natura Therapeutics, Inc. to screen for natural compounds that will target CD45 activation in the brain's immune cells," Dr. Bickford said.

The findings are published online in the Journal of Neuroscience. (ANI)