It may not be radioactive, but venom from a dangerous spider in Australia may help give researchers the super power of protecting brains from strokes.

Venom from the Australian funnel-web spider (Hadronyche infensa) contains a chemical that shuts down an ion channel known to malfunction in brain cells after strokes, researchers report Monday in PNAS. In cell experiments, the harmless chemical protected brain cells from a toxic flood of ions unleashed after a stroke strikes. In rats, the venom component markedly protected the rats’ brains from extensive damage—even when it was given hours after a stroke occurred.

That “translates to improved behavioral outcomes, with a marked decrease in neurological deficits and motor impairment.” This is according to the authors of the report, who are researchers at Australia’s University of Queensland and Monash University.

We’re still in the early days for a potential venom-based treatment. Researchers have years, if not decades, of work to figure out if their particular venom is safe and effective in humans. And very few potential therapies make the cut. But, this early study gives us reason to be somewhat optimistic: it follows years of research and hypotheses that such venom components and their ion channel-targets could be key to new stroke treatments—which are desperately needed.

Six million people die from strokes each year in the world, while five million more are left with permanent disabilities from them.

The vast majority of strokes involve a blockage that stops or slows the flow of blood into an area of the brain (other strokes can be caused by hemorrhages.) This leaves brain cells without fresh blood and oxygen. To cope, the cells can switch to metabolic pathways that don’t rely on oxygen. But this creates acidic conditions, and the pH outside of brain cells starts dropping fast—a scenario called acidosis. In the acidic, oxygen-starved brain regions, brain cells become damaged and start dying off, causing irreparable damage.

The only drug approved by the Food and Drug Administration to treat these types of strokes tries to restore blood flow by breaking up clots. But this drug is only used in about three to four percent of stroke victims because it has to be used within 4.5 hours of the stroke. It also comes with the risk of causing hemorrhages.

To find a better treatment, researchers are trying to work out all the details of what goes on in cells right after a stroke occurs and acidic conditions set in. In doing so, they’ve discovered that a group of ion channels, called acid-sensitive ion channels (ASICs), play a role. In fact, when researchers obliterate one type of ASICs—ASIC 1a—from the brains of mice, the rodents experience around 60 percent less damage from strokes than normal.

Researchers hypothesize that ASIC 1a can quickly sense slight changes in pH around brain cells after a stroke—then they start pumping. The ion channel conducts calcium ions and when ASIC 1a gets going it may inundate brain cells with calcium. This causes toxic, dire effects.

Years ago, researchers stumbled upon a chemical in tarantula venom that specifically blocks ASIC 1a. When researchers gave it to rats who had suffered strokes, it could significantly protect their rat brains from stroke-related damage.

In the new study, researchers spotted a similar peptide in the funnel web spider’s venom, which they dubbed Hi1a. When they tested the venom, they found that it, too, can inhibit ASIC 1a. But venom is much better at inhibiting ASIC 1a. The chemical is more potent and faster acting. In molecular experiments, it seemed to be able to clamp the ion channel closed before it even started pumping. In rats, the Hi1a venom protected up to 77 percent of cells: it rescued tissue in the most heavy-hit brain regions and limited peripheral damage. Plus, the spider venom showed protective effects in rat brains up to eight hours after they suffered a stroke. All the while, it showed no signs of causing harmful side-effects.

In all, the authors conclude, Hi1a venom is “a powerful pharmacological tool for probing the role of ASIC1a in acid-mediated neuronal injury and various neurological disorders, and a promising lead for the development of therapeutics to protect the brain...”

PNAS, 2017. DOI: 10.1073/pnas.1614728114 (About DOIs).