Australian scientists have made an amazing discovery with the potential to revolutionize stroke treatment.

A team of researchers from the University of Queensland and Monash University isolated a protein in the venom of the infamous funnel-web spider that can considerably reduce brain damage due to cerebrovascular accidents, even when administered eight hours after apoplexy.

This isn't the first time researchers pointed out tremendous health benefits can be reaped from the toxins of different venomous spiders.

Last year, the University of Queensland published two other studies on the therapeutic properties of spider venom, one detailing how the green velvet tarantula can help with chronic pain, the other suggesting tarantula venom can ease the discomfort of irritable bowel syndrome.

"We believe that we have, for the first time, found a way to minimize the effects of brain damage after a stroke," explained lead researcher Professor Glenn King in a university press release.

Why Funnel-Web Spiders?

Funnel-web spiders are among the world's deadliest arachnids, with extremely toxic venom that is potent enough to kill a human within 15 minutes.

Since the venom is designed to specifically target the prey's nervous system, King, from the Institute for Molecular Bioscience at the University of Queensland, wondered if it could be harnessed to reverse brain damage after a life-threatening event.

His team travelled to Fraser Island to investigate this hypothesis and brought back three Darling Downs funnel-web spiders (Hadronyche infensa) to be tested in the lab.

After engaging the spiders to make them release their toxin - by applying electric charges to their fangs and gathering the venom with a pipette, a process also known as "milking" - the scientists studied its chemical composition and found a harmless compound with the potential to save lives.

DNA sequencing of the venom revealed a molecule called Hi1a, which closely resembled another chemical known for its protective effects on brain cells. This prompted the team to synthesize the molecule and observe its properties, which proved to be even more effective than the compound that initially served as comparison.

What The Study Showed

Lab tests confirmed the molecule can halter neuron loss after a stroke by blocking ion channels in brain cells.

These channels are activated by the acid produced in the brain when it no longer receives oxygen and are responsible for most of the cell damage that occurs during a cerebrovascular accident.

A single dose of the Hi1a molecule was shown to reduce neuron damage by 80 percent when administered to rats two hours after an induced stroke.

The compound retains its protective properties even for a longer period, as researchers found it can restore neurological and motor functions by nearly 65 percent when dispensed eight hours after the stroke.

"Hi1a even provides some protection to the core brain region most affected by oxygen deprivation, which is generally considered unrecoverable due to the rapid cell death caused by stroke," said King.

The researchers detailed their findings in the journal Proceedings of the National Academy of Sciences. They are hoping to commence human trials of the Hi1a molecule in the next couple of years, pending further research.

In 85 percent of stroke cases, the damage is produced by a blockage in cerebral blood vessels, while the rest of cerebrovascular accidents are caused by hemorrhaging ruptured vessels. Hi1a had shown incredible results in the first type of stroke, and now researchers plan to determine whether the molecule is equally effective in the second type of cerebrovascular accidents.

Breakthrough In Stroke Treatment

Cerebrovascular accidents are the second largest cause of death worldwide after heart attacks, and claim the lives of nearly 6 million people every year. Current treatments rely either on clot-busting drugs when the stroke is caused by a blood clot, or endovascular thrombectomy, a surgical procedure that removes the clot from the brain.

With no available medication to protect stroke victims against neuron damage, the newly discovered molecule could greatly improve treatment plans, offering a safe and reliable alternative.

If future tests prove Hi1a can be also administered in cases of brain hemorrhage, the compound could reduce the number of fatalities and restore brain functions for stroke survivors.

"The drug could be given in the ambulance to most stroke patients before hospital arrival, maximizing the number of neurons that can be saved," said King.

According to Kate Holmes, from the Stroke Association, the treatments currently available require more urgency and must be administered in half the time as the Hi1a molecule, making the compound particularly beneficial for "people who are unable to arrive at hospital quickly."

"We welcome any treatment that has the potential to reduce the damage caused by stroke," said Holmes.

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