Alzheimer’s is a form of dementia, characterized by behavioral, thinking and memory dysfunction that is severe enough to impair intellectual ability. It is the most common type of dementia and accounts for 60-80% of all cases of dementia.
In the course of the disease, tangles and plaques start forming in the brain because of the amalgamation of atypical proteins which cause the deterioration of cognitive function in the patient.
Currently, around 50 million people worldwide suffer from the disease, and the number is projected to grow to more than 150 million in the next three decades. The costs associated with the medical and social care of patients is presently in the hundreds of billions of U.S dollars worldwide.
Although Alzheimer’s has commonly been attributed to old age seeing that most of the afflicted are 65 years or over, scientists have now found a link between the disease and blood glucose levels. It is the first time that a tipping point; a molecular link between Alzheimer’s and glucose in the blood has been established by scientists.
We know that obesity and diabetes are conditions that arise from hyperglycemia. Even though researchers knew that blood sugar glucose and its respective breakdown byproducts could impair intracellular proteins—glycation, they never quite understood it’s link to Alzheimer’s.
However, researchers have shown that an immunogenic enzyme is damaged by excess levels of glucose. It means that there is an increased risk of diabetics to be predisposed to the disease, unlike their healthy counterparts.
Researchers from the University of Bath and the Wolfson Center in King’s College London studied brain specimens from individuals who had Alzheimer’s and healthy individuals. By employing a delicate method to detect glycation, they discovered that at the onset of Alzheimer’s, the glycation process destroys a vital enzyme known as MIF—Macrophage Migration Inhibitory Factor.
MIF is crucial in immune reactions and plays a part in the regulation of insulin in the body. The enzyme is responsible for immunogenic response to the aggregation of atypical proteins in Alzheimer’s. The enzymes functional impairment during glycation is the tipping point to further advancement of the disease.
Additionally, the increase of glycation appears to be a direct consequence of the progression of Alzheimer’s. According to Jean Van Den Elsen, a professor at the University of Bath, the MIF enzyme is modified in patients at the onset of Alzheimer’s by glucose in the brain and scientists are now trying to investigate possible identical changes in the blood.
Dr. Rob Williams from the University of Bath added that knowledge of the molecular link would allow researchers to develop a chronological account of the progression of Alzheimer’s and hopefully facilitate the detection of individuals who are at risk. Furthermore, it will provide a blueprint for possible preventative treatment.
According to Dr. Omar Kassaar, this discovery will hopefully add emphasis on the need for controlling dietary sugar intake seeing that excess sugar not only predisposes us to obesity and diabetes but also to Alzheimer’s.
Dunhill Medical Trust funded the research study, and the human brain specimens used were provided by BDR ( Brains for Dementia Research)—a collective between the Medical Research Council, Alzheimer’s Society and Alzheimer’s Research UK.