While sequencing the DNA of toxins found in the venom of one of the world's deadliest spiders, researchers recently discovered a molecule that may help prevent brain damage following a stroke. The study, which was done on rats, adds to a growing body of research on the medical potential of animal venom: Snake venom, for instance, may be able to help us treat pain. Tarantula venom shows promise for helping people with IBS and chronic pain. Wasp venom killed cancer cells in petri dish studies, and platypus venom contains a hormone that regulates glucose, which has drawn the interest of diabetes researchers.
In this case, the venom being studied belongs to a Darling Downs funnel-web spider, which is found in eastern Australia. Within its venom, researchers identified a molecule called Hi1a, which bears a resemblance to two other molecules shown to help protect brain cells. That led them to synthesize the molecule and see if had similar properties—and they found it could provide what they call "potent neuroprotection."
That's important because, the researchers note, strokes kill about 6 million people a year; after heart attacks, stroke is the second-leading cause of death worldwide. Another 5 million stroke victims survive but are left with a permanent disability. And stroke makes the brain vulnerable even after the initial event: Oxygen deprivation causes a severe drop in brain pH, leading to damaged neurons. That neuronal damage often leads to progressive cognitive decline and dementia, meaning many patients never fully recover.
To date there's been no drug to mitigate that initial damage. Hi1a could help fix that by changing how the brain responds to a stroke. A stroke happens when blood flow to the brain is interrupted, either by a blockage or by a rupture. Blood carries oxygen to the brain; without it, the oxygen level drops, forcing the brain into a process called anaerobic glycolysis. That can keep the brain functioning in the short term, but produces acid (from that lowered pH) that can kill brain cells.
Scientists have already been able to mediate this effect by genetically modifying rodents. That's great for understanding the basic science, but obviously isn't applicable in humans. Hi1a, though, could offer a different approach. Using rats, researchers have shown that it successfully blocks certain ion channels in cells—those that respond to the acidic conditions in the brain following a stroke. That led to less brain damage; in fact, delivered within two hours after the stroke, it reduced damage by 80 percent. Even delivered eight hours after the stroke, the studies showed about a 65 percent reduction. One researcher told the Guardian that while the control rats were profoundly damaged, for the other group, treatment with Hi1a "almost restored these functions to normal."
That doesn't mean we can just start trying it on humans, of course. Further tests will see whether it works in all cases, and whether it's safe in strokes that are caused by ruptures as well as by blockages. After that, researchers would like to begin testing in humans within two years. If testing proves successful, Hi1a could be a first step in treating one of the most frustrating and intractable aspects of a stroke.