Snake venom may hold key to breaking down plaques that cause Alzheimer's disease

March 2, 2016
Snake venom may hold key to breaking down plaques that cause Alzheimer’s disease

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 patients with the disease, these enzymes appear unable to adequately perform their actions, causing the toxic protein to accumulate into plaque deposits, which many researchers consider 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 are just starting to accumulate.

Monash researchers have discovered what could well be this elusive drug candidate– a molecule in that appears to activate the enzymes involved in breaking down the amyloid plaques in the brain that are the hallmark of Alzheimer's disease. Dr Sanjaya Kuruppu and Professor Ian Smith from Monash University's Biomedicine Discovery Institute have just published their research in Nature Scientific Reports.

Dr Kuruppu has spent most of his research life studying snake venoms, looking for drug candidates.  When he began researching Alzheimer's disease he says that "snake venom was an obvious place for me to start."

He was looking for a molecule that would stimulate the enzymes to break down the amyloid plaques.  What he found, when screening various snake venoms, was in fact one 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. Dr Kuruppu and his team have developed synthetic versions of this molecule. Initial tests done in the laboratory using human cells have shown it to have the same effects as the native version found in the snake venom.

Dr Kuruppu is one of the four researchers in Australia to receive funding from the National Foundation for Medical Research and Innovation to conduct further testing of this newly-identified molecule.

Explore further: Hyperactive neurons may be culprit in Alzheimer's

More information: A. Ian Smith et al. N-terminal domain of Bothrops asper Myotoxin II Enhances the Activity of Endothelin Converting Enzyme-1 and Neprilysin, Scientific Reports (2016). DOI: 10.1038/srep22413

Related Stories

Hyperactive neurons may be culprit in Alzheimer's

January 13, 2016

A long-term reduction in neuronal activity reduces amyloid plaques associated with Alzheimer's disease, Yale University researchers have found. The study, using mouse models of Alzheimer's, found the opposite is also true—triggering ...

Alzheimer protein's structure may explain its toxicity

May 7, 2015

Researchers at the University of Illinois at Chicago have determined the molecular structure of one of the proteins in the fine fibers of the brain plaques that are a hallmark of Alzheimer's disease. This molecule, called ...

Recommended for you

Research finds that ultrasound slows brain ageing

October 12, 2016

Treatment with scanning ultrasound has already been proven to reverse Alzheimer's disease in mice, and now it appears it could also slow down ageing in healthy brains, according to University of Queensland research.


Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.