New anti-inflammatory drug reduces death of existing brain cells then repairs damage after stroke

Researchers at The University of Manchester have discovered that a potential new drug reduces the number of brain cells destroyed by stroke and then helps to repair the damage.

A reduction in blood flow to the brain caused by stroke is a major cause of death and disability, and there are few effective treatments.

A team of scientists at The University of Manchester has now found that a potential new stroke drug not only works in rodents by limiting the death of existing brain cells but also by promoting the birth of new neurones (so-called neurogenesis).  

This finding provides further support for the development of this anti-inflammatory drug, interleukin-1 receptor antagonist (IL-1Ra in short), as a new treatment for stroke. The drug is already licensed for use in humans for some conditions, including rheumatoid arthritis. Several early stage clinical trials in stroke with IL-1Ra have already been completed in Manchester, though it is not yet licensed for this condition.

In the research, published in the biomedical journal Brain, Behavior and Immunity, the researchers show that in rodents with a stroke there is not only reduced brain damage early on after the stroke, but several days later increased numbers of new neurones, when treated with the anti-inflammatory drug IL-1Ra.

Previous attempts to find a drug to prevent brain damage after stroke have proved unsuccessful and this new research offers the possibility of a new treatment.

Importantly, the use of IL-1Ra might be better than other failed drugs in stroke as it not only limits the initial damage to brain cells, but also helps the brain repair itself long-term through the generation of new brain cells.

These new cells are thought to help restore function to areas of the brain damaged by the stroke. Earlier work by the same group showed that treatment with IL-1Ra does indeed help rodents regain motor skills that were initially lost after a stroke. Early stage clinical trials in stroke patients also suggest that IL-1Ra could be beneficial.

The current research is led by Professor Stuart Allan, who commented: "The results lend further strong support to the use of IL-1Ra in the treatment of stroke, however further large trials are necessary."

Preliminary findings suggest a drug used to treat   cryopyrin-associated periodic syndromes  disease might also reduce painful flare-ups in gout patients starting new medication regimens.

In a new study, the protein-inhibitor drug rilonacept (Arcalyst) appeared to markedly lower the risk of gout flare-ups during the first few months of treatments aimed at lowering uric acid levels.

"To reduce deposits of crystals in the joints, we advise patients to initiate treatment with medications that lower levels of uric acid in the blood," study author Dr. H. Ralph Schumacher 

The researchers wanted to learn if rilonacept could lower this short-term risk for by neutralizing a specific target protein -- interleukin 1 or IL-1 -- before it initiates inflammation.

They looked at 83 gout patients in 27 U.S. study centers who had a history of gout flare-ups and high levels of uric acid. All were placed on a chronic uric-acid lowering regimen of the standard drug allopurinol.

About half were also given an initial double-dose injection of rilonacept (320 milligrams) followed by a single dose for 16 weeks. The other half received sugar pills.

Rilonacept patients were less likely to have flare-ups, with 15 percent experiencing flare-ups three-months into the study compared with 45 percent among the non-rilonacept group, the researchers found....

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