Arthritis protein linked to Alzheimer's treatmentIt reverses cognitive impairment, research finds
A protein linked to rheumatoid arthritis has been found to reduce the symptoms of Alzheimer's disease, according to new research. A commercially available treatment for cancer might be soon tested to establish if it can be used to treat Alzheimer's.
The study, conducted on mice, found that a signaling protein released during rheumatoid arthritis stimulates the body's scavenger cells to remove brain deposits of a protein called amyloid, which is associated with Alzheimer's.
Rheumatoid arthritis is a chronic disease which leads to inflammation of the joints and surrounding tissue. Those affected are less likely to develop Alzheimer's, an incurable, degenerative disease that is the most common form of dementia.
"Our findings provide a compelling explanation for why rheumatoid arthritis is a negative risk factor for Alzheimer's disease," said principal investigator Huntington Potter, professor of molecular medicine at the University of South Florida.
A recombinant human form of the signaling protein GM-CF is approved by the US Food and Drug Administration under the brand name Leukine, and has been used for years to treat certain cancer patients who need to generate more immune cells, Dr Potter said.
"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 research was conducted on mice genetically altered to show memory problems exhibited by Alzheimer's patients. The mice who were treated with the GM-CSF protein performed much better on tests that measured their working memory and learning - in fact, they compared to the performance of mice without dementia.
"We were pretty amazed that the treatment completely reversed cognitive impairment in 20 days," said Dr Tim Boyd, one of the lead authors.
The study also found that the brains of Alzheimer's mice treated with the GM-CSF protein showed more than a 50 per cent decrease in beta amyloid, a substance that forms the plaques that are a hallmark of Alzheimer's disease.
This reduction, and the improvement in memory, was accompanied by an increase in cells called microglia in the brain. These cells work on inflamed or damaged areas to remove toxic substances.
The scientists believe that the GM-CSF protein recruits more microglia into the brain to remove Alzheimer's plaques.
The USF Health Byrd Alzheimer's Institute plans to begin a pilot clinical trial later this year investigating the GM-CSF protein in patients with mild or moderate Alzheimer's disease.
The study appears online in the Journal of Alzheimer's Disease.
This article was published on Mon 23 August 2010
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