Diabetes’ link with Alzheimer’s disease identified
London, Have a sweet tooth? Beware, you may be at risk of developing Alzheimer’s disease, as a study has found a specific molecular link between abnormally high blood sugar levels, or hyperglycaemia — a key characteristic of diabetes and obesity — and Alzheimer’s disease.
The findings showed that excess glucose damages a vital enzyme involved with inflammation response to the early stages of Alzheimer’s and that is the reason behind diabetes patients having an increased risk of developing the disease compared to healthy individuals.
“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 sugar intake in our diets,” said Omar Kassaar, from the University of Bath in Britain.
For the study, published in the journal Scientific Reports, the team studied brain samples from people with and without Alzheimer’s using a sensitive technique to detect glycation — the bonding of a sugar molecule.
The results showed 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 build-up of abnormal proteins in the brain during Alzheimer’s. This inhibition and reduction of MIF activity caused by glycation could be the “tipping point” in disease progression, the researchers 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,” explained Jean van den Elsen, Professor at the University of Bath.
The study may be vital to developing a chronology of how Alzheimer’s progresses and help identify those at risk of Alzheimer’s and lead to new treatments or ways to prevent the disease, the researchers noted.