Researchers at Simon Fraser University have now created a molecule they call Thiamet-G to stop the action of the O-GlcNAcase enzyme, and thus, prevent depletion of the sugar molecules to stop clumping of Tau; a potential effective treatment for Alzheimer’s.
For long, it has been known that structures in the brain called microtubules require the molecule Tau to remain stable. The microtubules are concerned with transmission of signals through cells and their proper functioning is essential to brain activity.
The Tau protein molecules are invariably linked with certain sugar molecules and presence of this sugar is essential for the proper functioning of the microtubules and ultimately, the brain.
Previous researchers have also found that in an Alzheimer’s brain, the sugar is removed by an enzyme called O-GlcNAcase, causing clumping of the Tau and greater the number of such clumps, more severe is the Alzheimer’s.
Working with his graduate students at the SFU Laboratory of Chemical Glycobiology, David Vocadlo has found that administering Thiamet-G to mice blocks the action of the O-GlcNAcase enzyme.
This was evident from the lesser proportion of clumping of Tau in these animals, along with healthier brain function.
Explaining this finding published in the journal Nature Chemical Biology, Vocadlo said:
“This work shows targeting the enzyme O-GlcNAcase with inhibitors is a new potential approach to treating Alzheimer’s. This is vital since to date there are no treatments to slow its progression. In the short term, we need to develop better inhibitors of the enzyme and test them in mice. Once we have better inhibitors, they can be clinically tested.”
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