Excess sugar (hyperglycemia) is well known to be bad for us when it comes to diabetes and obesity, but a potential link between excessive sugar and Alzheimer’s disease may be 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 and death. Globally there are around 50 million people with Alzheimer’s disease, and this figure is predicted to rise to more than 125 million by 2050. The global social cost of this disease runs into the hundreds of billions of dollars when accounting for not only the cost of medical care for these patients but also the cost related to social care.
So how did excessive sugar become identified as a risk factor for Alzheimer’s disease? The concern stemmed from the observation that diabetics have an increased risk of developing Alzheimer’s disease compared to healthy individuals. Despite this observation, the actual physiological link between excessive sugar and Alzheimer’s disease has been evasive. 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.
But now scientists from the University of Bath Departments of Biology and Biochemistry, Chemistry and Pharmacy and Pharmacology, working with colleagues at the Wolfson Centre for Age Related Diseases, King’s College London, have unraveled the molecular link between blood sugar, glucose, and Alzheimer’s disease. Their research has recently shown that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer’s.
By studying brain samples from people with and without Alzheimer’s using a sensitive technique to detect glycation, the team 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.
Hopefully, this latest research will be vital to developing a chronology of how Alzheimer’s progresses and will help identify those at risk of Alzheimer’s and lead to new treatments or ways to prevent the disease.
(This research study was funded by the Dunhill Medical Trust. Human brain tissue for this study was provided through Brains for Dementia Research, a joint initiative between Alzheimer’s Society and Alzheimer’s Research UK in association with the Medical Research Council. The work is published in the journal, Scientific Reports.)