A protein released during rheumatoid arthritis lessened the intensity of Alzheimer's disease in mice in a recent experiment.
University of South Florida researchers found that the protein, GM-CSF, likely stimulates the body's natural scavenger cells to attack and remove Alzheimer's amyloid deposits in the brain.
AdvertisementThe USF researchers are among the first to look at what effect innate immunity gone awry in rheumatoid arthritis may play in protecting against Alzheimer's disease.
"Our findings provide a compelling explanation for why rheumatoid arthritis is a negative risk factor for Alzheimer's disease," said Huntington Potter of USF Health Byrd Alzheimer's Institute.
"Moreover, the recombinant human form of GM-CSF (Leukine) is already approved by the FDA and has been used for years to treat certain cancer patients who need to generate more immune cells," said Potter.
"Our study, along with the drug's track record for safety, suggests Leukine should be tested in humans as a potential treatment for Alzheimer's disease," he added.
The researchers analyzed three rheumatoid arthritis growth factors in mouse models and identified the signaling protein GM-CSF as the most promising for potential protective benefit against Alzheimer's disease.
Then, they peripherally injected GM-CSF into two groups of mice - those genetically altered to develop memory problems mimicking Alzheimer's disease and normal, aged mice.
Behavioral tests confirmed the Alzheimer's mice were exhibiting signs of memory impairment at age 12 months. Another two control groups of mice - the Alzheimer's mice and normal mice - were administered saline (placebo).
After the 10th day of injections, all the mice began a series of behavioral testing. At the end of the 20-day study, the cognitively impaired mice treated with GM-CSF performed substantially better on tests measuring their working memory and learning.
"We were pretty amazed that the treatment completely reversed cognitive impairment in 20 days," said Tim Boyd, who, together with Steven Bennett, is a study lead author.
In addition, the brains of GM-CSF-treated Alzheimer's mice showed more than a 50-percent decrease in beta amyloid, a substance forming the sticky clumps of plaques that are a hallmark of Alzheimer's disease.
The study appeared in the journal Alzheimer's Disease.
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