Study uncovers a connection between hyperglycaemia and Alzheimer's disease


According to a study published in the journal Scientific Reports, researchers at the University of Bath have made a breakthrough in understanding the pathogenesis of Alzheimer's disease, the most common type of dementia. Specifically, they have found that increased levels of blood sugar may contribute to the development of Alzheimer's. This is the first time that scientists have identified a clear relationship between Alzheimer's and blood glucose level.

Hyperglycaemia is a term that describes a condition in which too much glucose is circulating in the blood. Hyperglycaemia is a serious problem in obesity and diabetes. Left untreated, hyperglycaemia can eventually lead to complications affecting various organs and tissues such as the eyes, kidneys, and nerves. There is evidence that diabetics are more likely to develop Alzheimer's than healthy individuals. But to date, little is known about the precise connection between hyperglycaemia and Alzheimer's.

Glucose and its metabolites can damage proteins in cells through a non-enzymatic reaction called glycation. This is associated with the pathogenesis of Alzheimer's and is also a characteristic of the hyperglycaemia caused by diabetes. Jean van den Elsen and colleagues at the University of Bath collaborated with Paul T. Francis from King's College London to uncover the relationship between glucose and Alzheimer's. Using a method called Flu-PAGE, they analyzed the brain samples of both Alzheimer's patients and age-matched control subjects. By doing so, the researchers defined an early glycation profile of human brain, and found that in the early stage of Alzheimer's glycation damages the Macrophage migration inhibitory factor (MIF).

MIF is a unique cytokine and has enzymatic activity. Earlier studies have identified it as a regulator of innate immunity. Specifically, MIF is a part of the host antimicrobial alarm system and stress response that promotes the pro-inflammatory functions of immune cells. In an Alzheimer's brain, MIF is involved in immune response to the accumulation of abnormal proteins.

The researchers assumed that inhibition and reduction of MIF activity caused by glycation could contribute to the development of Alzheimer's. The study suggests that glucose modified MIF could be a molecular link between hyperglycaemia and the dysregulation of the innate immune system in AD.
 
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