Targeting Inflammation May Protect and Restore the Brain after Stroke

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Many researchers are currently investigating other compounds related to immune responses, both short- and long-term. For example, Fagan and her colleagues recently discovered that although administering a molecule called compound 21, which binds to certain hormone receptors in the brain, did not reduce brain damage after stroke—it did lead to less cognitive impairment weeks later. “This is probably not due to early neuroprotection but [an effect on] ongoing inflammation after stroke,” she says.

Addressing inflammation is one of many different approaches to protecting the post-stroke brain. Scientists have attempted—and are still trying—to target other processes including the production of free radicals (highly reactive molecules) or excitotoxicity (neuron death caused by overactivity of chemical messengers in the brain). Some researchers are starting to revisit drugs that have previously failed in clinical trials. Neurologist Gregory Bix at the University of Kentucky believes that, as in the case of complement inhibition, “one of the issues with these agents was, quite simply, that they weren’t getting where they needed to be.”

Bix hopes administering neuroprotective agents alongside a thrombectomy—right at the site of the injury—may vastly increase beneficial effects. He and his colleagues are now conducting clinical trials to investigate whether repurposing drugs might work using this type of system. “I’m very excited about the potential of neuroprotective therapies to make a comeback,” he says.

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