You already know that sugar isn't the best thing for your health, but new research out of England might just give you another reason to avoid the white stuff. Scientists there say they've discovered a molecular link between blood sugar levels and an enzyme that just might be the tipping point in Alzheimer's disease.

Researchers from the University of Bath (UB) and King's College London, studied brain samples from people who have Alzheimer's disease and from those who don't. Working with the previously discovered link between sugar and cell damage, they developed a way to tag sugar-damaged proteins with a fluorescing marker.

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By tracking the glowing markers, the researchers were able to see that in the early stages of Alzheimer's, excess sugar in the blood damages an enzyme called macrophage migration inhibitory factor (MIF), through a process called glycation.

When MIF is functioning properly in the brain, it can help fight against build up of abnormal proteins that clump and lead to the plaques that are a hallmark of Alzheimer's. But when the enzyme is damaged, it can't play this vital role in keeping plaques from developing. The researchers found that as the disease progresses, the glycation of the enzymes increases, showing that as this first defense falls, the disease becomes more unfettered.

"Normally MIF would be part of the immune response to the build-up of abnormal proteins in the brain, and we think that because sugar damage reduces some MIF functions and completely inhibits others that this could be a tipping point that allows Alzheimer's to develop," said UB professor Jean van den Elsen.

"Excess sugar is well known to be bad for us when it comes to diabetes and obesity, but this potential link with Alzheimer's disease is yet another reason that we should be controlling our sugar intake in our diets," added UB's Omar Kassaar.

The researchers are hopeful that their work will help them further fill out the timeline of how Alzheimer's progresses and uncover a new course of attack to treat or prevent the disease. Their findings have been published in the journal Nature.

Source: University of Bath