AsianScientist (Mar. 14, 2016) – Researchers based in Australia have discovered a molecule in snake venom that appears to activate the enzymes that break down amyloid plaques in the brain—a hallmark of Alzheimer’s disease. The work was published in Scientific Reports.
A toxic protein called amyloid beta is thought to play a key role in the onset of Alzheimer’s disease. In healthy people, amyloid beta is degraded by enzymes as it forms. However, in those patients with the disease, it appears as though these enzymes are unable to adequately perform their actions so that this toxic protein ends up accumulating into plaque deposits, which many researchers think leads to dementia.
One of the Holy Grails of the pharmaceutical industry has been to find a drug that stimulates these enzymes in people, particularly those who are in the early stages of dementia when amyloid plaques are just starting to accumulate.
Corresponding author Dr. Sanjaya Kuruppu of Monash University’s Biomedicine Discovery Institute and colleagues were looking for a molecule that would stimulate the enzymes to break down the amyloid plaques.
“Snake venom was an obvious place for me to start,” said Kuruppu.
What he found when screening various snake venoms was a molecule with the ability to enhance the activity of two plaque-degrading enzymes. This molecule was extracted from a venom of a pit viper found in South and Central America.
After developing synthetic versions of this molecule and initial tests done in the laboratory using human cells, the team’s findings have shown it to have the same effects as the native version found in the snake venom.
The article can be found at: Smith et al. (2016) N-terminal domain of Bothrops asper Myotoxin II Enhances the Activity of Endothelin Converting Enzyme-1 and Neprilysin.
Source: Monash University; Photo: Rushen/Flickr/CC.
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