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

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, Johannes Van Den Elsen

Research output: Contribution to journalArticle

16 Citations (Scopus)

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.
Original languageEnglish
Article number42874
Pages (from-to)1-12
Number of pages12
JournalScientific Reports
Volume7
DOIs
Publication statusPublished - 23 Feb 2017

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