22 August 2010 Last updated at 23:04 GMT BBC Online By Caroline Parkinson Health reporter, BBC News 
Rheumatoid arthritis is caused by the immune system attacking the body's own tissues
A protein produced in cases of rheumatoid arthritis appears to protect against the development of Alzheimer's disease, US scientists have said.
In the Journal of Alzheimer's Research study, mice with memory loss given the protein fared better in tests.
A synthetic version of GM-CSF protein is already used as a cancer treatment.
UK experts said the study was "an important first step" and tests were needed to see if the drug worked for people with Alzheimer's.
In people with rheumatoid arthritis, the immune system goes into "overdrive" and produces attacking proteins - including GM-CSF.
Rubbish collectors It had already been recognised that people with rheumatoid arthritis were less likely to develop Alzheimer's, but the protective link had been thought to be due to non-steroidal anti-inflammatory drugs (NSAIDs) taken by people with the condition.
However tests showed this was not the case.
In this study, University of South Florida researchers genetically altered mice to have memory problems similar to those seen in Alzheimer's disease, which is a form of dementia.
They then treated them - and some healthy mice - with the protein. Other mice - both healthy ones and those with Alzheimer's symptoms - were given a dummy (placebo) treatment.
At the end of the 20-day study, the Alzheimer's mice treated with GM-CSF fared substantially better on tests measuring memory and learning, and performed at a similar level to mice of the same age without the condition.
Even the healthy mice treated with GM-CSF performed slightly better than their untreated peers.
Mice with Alzheimer's that were given the placebo continued to do poorly in the tests.
The researchers have suggested the protein may attract an influx of cells called microglia from the peripheral blood supply around the brain, which then attack the characteristic plaques that form in people with Alzheimer's.
Microglia are like the body's natural "rubbish collectors" that go to damaged or inflamed areas to get rid of toxic substances.
The brains of GM-CSF-treated Alzheimer's mice showed more than a 50% decrease in beta amyloid, the substance which forms Alzheimer's plaques.
The researchers also observed an apparent increase in nerve cell connections in the brains of the GM-CSF-treated mice, which they say could be a reason memory decline was reversed.
'Crucial next stage' Dr Huntington Potter, who led the research at the University of South Florida's Health Byrd Alzheimer's Institute, said: "Our findings provide a compelling explanation for why rheumatoid arthritis is a negative risk factor for Alzheimer's disease."
An artificial version of GM-CSF, a drug called Leukine, is already approved by the US Food and Drug Administration and has been used to treat cancer patients who need to generate more immune cells.
Dr Potter added. "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."
Dr Simon Ridley, head of research at the UK's Alzheimer's Research Trust, said: "Positive results in mice can be an important first step for any new treatment, and it's encouraging the team is already planning the crucial next stage of a trial in people.
"We won't know whether GM-CSF can help people with Alzheimer's until clinical trials are completed".
Dr Susanne Sorensen, head of research at the Alzheimer's Society, said: "This exciting research provides a possible answer to the long, unexplained question of why rheumatoid arthritis could reduce the risk of Alzheimer's disease.
"Given the identified protein is already available as a drug that is proven to be safe in humans, the time taken to develop an Alzheimer's disease treatment could be substantially reduced.
"However, we must not jump the gun. Much more research is needed before we can say for certain that the findings demonstrated in mice would also occur in humans."
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