Can spider venom protect your brain?

Its name: Hadronyche infensa or the “Darling Downs funnel web spider” (the name of a vast farming area in Australia): a very toxic poisonous spider. But this creature may also have an unexpected virtue: protecting the brain from neural damage caused by a stroke. How did Australian researchers chance upon this discovery? Read on to find out more about this study published in PNAS.

One of the studies main authors, Professor Glenn King from the Institute for Molecular Bioscience at the University of Queensland (Australia) says, “We believe that we have, for the first time, found a way to minimize the effects of brain damage after a stroke.” These encouraging remarks are the result of the discovery of a protein that the scientists have named “Hi1a.” It’s in sequencing the genome of the toxins present in the spider Hadronyche infensa that scientists were able to isolate this molecule and test its neuro-protective virtues in rats that had suffered a stroke. According to the preclinical studies, administering a single dose of the protein up to eight hours after the stoke induced a two-fold positive action: it protected the brain tissue and improved neurological performance, and it even provided a protective barrier to the core area of the brain that had been deprived of oxygen. The Hi1a protein appears to block the ion channel 1a, which is largely responsible for the brain damage in cases of stroke.

Caution is advised as we're still a long way away from a potential treatment. While the researchers appear confident and hope to be able to conduct clinical trials on human patients in the next two years, there is no guarantee that the neuroprotective virtues of Hi1a will extend to humans.

Nevertheless, this research demonstrates the value of this important area of study (the potential virtues of toxins and venoms) for developing drugs.
Source: Irène R. Chassagnon and coll., “Potent neuroprotection after stroke afforded by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a,” in PNAS vol. 114 n°14, February 2017.


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