Abnormally high blood sugar, also known as hyperglycaemia, is a well-known characteristic of diabetes and obesity, but its link to Alzheimer’s disease is less familiar.
In a new study, published in the Journal Scientific Reports, researchers aimed to define an early ‘glycation profile’ of the human brain using specialised lab techniques.
Researchers already knew that glucose and its break-down products can damage proteins in cells via ‘glycation’ but the specific molecular link between glucose and Alzheimer’s disease was not understood.
This is where defining the ‘glycation profile’ was really important – or in other words, they wanted a better understanding the how sugars work at a cellular levels.
The researchers, based in the UK, analysed the brain samples from people with and without Alzheimer’s disease using a sensitive technique to detect glycation. The team discovered that in the early stages of Alzheimer’s disease, glycation damages an enzyme called MIF (macrophage migration inhibitory factor) which plays a role in immune response and insulin regulation.
Professor Jean van den Elsen, from the University of Bath said “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”.
MIF is involved in the response of brain cells to the build-up of abnormal proteins in the brain during Alzheimer’s disease. It appears that as Alzheimer’s progresses, glycation of these enzymes increases.
These research findings implicate MIF as a specific target of events which may lead to 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.
The findings suggest a new link between diabetes and dementia, which should continue to be researched.