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Abstract Title:

Macrophage Migration Inhibitory Factor is subjected to glucose modification and oxidation in Alzheimer's Disease.

Abstract Source:

Sci Rep. 2017 Feb 23 ;7:42874. Epub 2017 Feb 23. PMID: 28230058

Abstract Author(s):

Omar Kassaar, Marta Pereira Morais, Suying Xu, Emily L Adam, Rosemary C Chamberlain, Bryony Jenkins, Tony James, Paul T Francis, Stephen Ward, Robert J Williams, Jean van den Elsen

Article Affiliation:

Omar Kassaar

Abstract:

Glucose and glucose metabolites are able to adversely modify proteins through a non-enzymatic reaction called glycation, which is associated with the pathology of Alzheimer's Disease (AD) and is a characteristic of the hyperglycaemia induced by diabetes. However, the precise protein glycation profile that characterises AD is poorly defined and the molecular link between hyperglycaemia and AD is unknown. In this study, we define an early glycation profile of human brain using fluorescent phenylboronate gel electrophoresis and identify early glycation and oxidation of macrophage migration inhibitory factor (MIF) in AD brain. This modification inhibits MIF enzyme activity and ability to stimulate glial cells. MIF is involved in immune response and insulin regulation, hyperglycaemia, oxidative stress and glycation are all implicated in AD. Our study indicates that glucose modified and oxidised MIF could be a molecular link between hyperglycaemia and the dysregulation of the innate immune system in AD.

Study Type : In Vitro Study

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