An experimental model of Alzheimer’s disease has been successfully treated with a commonly used anti-inflammatory drug, mefenamic acid. Scientists from the University of Manchester found that the drug, which is routinely used for period pain, completely reversed memory loss and brain inflammation in mice.
Around 500,000 people in the UK have Alzheimer’s disease which gets worse over time, affecting many aspects of their lives, including the ability to remember, think and make decisions.
Transgenic mice, created to develop symptoms of Alzheimers disease, we’re used with one group of 10 treated with mefenamic acid, 10 treated with a placebo.
Though this is the first time a drug has been shown to target this inflammatory pathway, highlighting it’s importance in the disease model, Dr Brough, who led the study, cautions that more research is needed to identify it’s impact on humans, and the long-term implications of it’s use.
The research, funded by the Medical Research Council and the Alzheimer’s Society, paves the way for human trials which the team hope to conduct in the future.
Dr Brough commented, “There is experimental evidence now to strongly suggest that inflammation in the brain makes Alzheimer’s disease worse. Our research shows for the first time that mefenamic acid can target an important inflammatory pathway called the NLRP3 inflammasome, which damages brain cells.”
He added, “Until now, no drug has been available to target this pathway, so we are very excited by this result. However, much more work needs to be done until we can say with certainty that it will tackle the disease in humans as mouse models don’t always faithfully replicate the human disease.
“We are now preparing applications to perform early phase II trials to determine a proof-of-concept that the molecules have an effect on neuroinflammation in humans.”
Dr Doug Brown, Director of Research and Development at Alzheimer’s Society, added, “Testing drugs already in use for other conditions is a priority for Alzheimer’s Society it could allow us to shortcut the fifteen years or so needed to develop a new dementia drug from scratch.
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