Arthritis clue leads to fresh hope over dementia

Rheumatoid arthritis sufferers have a built-in protection against Alzheimer's that could soon become a promising new treatment for the brain disease.

The protein GM-CSF plays a role in the defective immune system response that leads to the arthritic disorder.

But it also marshals the immune system to remove harmful deposits in the brain that are linked to Alzheimer's.

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Tests on mice showed that the protein could reverse Alzheimer's symptoms in just 20 days. Scientists, who say they are "amazed" at the finding, believe the discovery could quickly lead to a practical new treatment for Alzheimer's.

A laboratory-made version of GM-CSF called Leukine has been used for years to boost the immune systems of some cancer patients. Because its safety profile is already well known, it should not take long to convert into an Alzheimer's therapy.

The US scientists, from the Health Byrd Alzheimer's Institute at Florida State University, are now planning a pilot trial later this year that will put the theory to the test.

Lead researcher Professor Huntington 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."

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It was already known that people with rheumatoid arthritis (RA), an auto-immune disease that attacks the joints, had a reduced risk of Alzheimer's.

Until recently, most experts assumed this was due to the anti-inflammatory drugs commonly given to RA sufferers. But recent clinical trials showed the drugs do not help Alzheimer's patients.

Prof Potter's team decided to investigate immune system mechanisms in RA.

"Our findings provide a compelling explanation for why rheumatoid arthritis is a negative risk factor for Alzheimer's disease," said the professor, whose research is published online today in the Journal of Alzheimer's Disease.

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Three RA proteins were studied in mice bred to develop the rodent equivalent of human Alzheimer's.

One, GM-CSF, proved most likely to be protective against the dementia condition.

The researchers then injected the protein into "Alzheimer's" mice, and normal old-age mice.

After 20 days, the treated Alzheimer's mice were performing substantially better in tests measuring their working memory and learning ability than those not given the protein.

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Even normal mice treated with GM-CSF performed slightly better than their untreated peers.

Dr Tim Boyd, another member of the Florida team, said: "We were pretty amazed that the treatment completely reversed cognitive impairment in 20 days."

The brains of GM-CSF-treated mice showed a more than 50 per cent decrease in the sticky clumps of protein that build up in the brains of Alzheimer's sufferers and are a hallmark of the disease.

The drug boosted numbers of scavenging immune cells known as microglia in the brain which get rid of toxic substances. The scientists believe GM-CSF stimulates microglia to attack and remove beta-amyloid deposits.

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