Excess Glucose Linked to Alzheimer’s Disease

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27 Feb 2017 --- A molecular link between the blood sugar glucose and Alzheimer's disease has been established by scientists, who have shown that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer's.

The findings have prompted researchers to further warn of the danger of too much sugar in the diet.

Abnormally high blood sugar levels, or hyperglycaemia, is well-known as a characteristic of diabetes and obesity, but its link to Alzheimer's disease is less familiar.

Diabetes patients have an increased risk of developing Alzheimer's disease compared to healthy individuals.

Dr Omar Kassaar, from the University of Bath, said: “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.”

In Alzheimer's disease, abnormal proteins aggregate to form plaques and tangles in the brain which progressively damage the brain and lead to severe cognitive decline.

Scientists already knew that glucose and its break-down products can damage proteins in cells via a reaction called glycation but the specific molecular link between glucose and Alzheimer's was not understood.

However, by studying brain samples from people with and without Alzheimer's using a sensitive technique to detect glycation, scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology discovered that in the early stages of Alzheimer's glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.

MIF is involved in the response of brain cells called glia to the build-up of abnormal proteins in the brain during Alzheimer's disease, and the researchers believe that inhibition and reduction of MIF activity caused by glycation could be the 'tipping point' in disease progression.

It appears that as Alzheimer's progresses, glycation of these enzymes increases.

Professor Jean van den Elsen, from the University of Bath Department of Biology and Biochemistry, said: “We've shown that this enzyme is already modified by glucose in the brains of individuals at the early stages of Alzheimer's disease. We are now investigating if we can detect similar changes in blood.”

“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.

Dr Rob Williams, also from the Department of Biology and Biochemistry, added: “Knowing this will be vital to developing a chronology of how Alzheimer's progresses and we hope will help us identify those at risk of Alzheimer's and lead to new treatments or ways to prevent the disease.”

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