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Myalgic Encephalomyelitis/Chronic Fatigue syndrome

 

Professor Tate’s ME/CFS research programme for 2019

(A) Energy production

We are determining in ME/CFS patients and age/gender matched healthy controls the complete bioenergetic profiles of the cell’s energy powerhouse (mitochondrion) and its effectiveness to produce energy. This will include the levels of an important component of this energy production, CoQ10, in plasma and immune cells and whether the energy production can be improved by the freely available supplement MitoQ. We will also determine how concentrations of CoQ10 change in the plasma and cells of patients when they begin to take the supplement. In both cases we will determine if there is an improvement in bioenergetic profiles in response to MitoQ. Production of destructive reactive oxygen species, and the effectiveness of MitoQ as an antioxidant to mitigate this thereby improving energy production will be assessed. Key features of ME/CFS like relapse/recovery and post exertional malaise will be studied.

(B) Epigenetic code dynamics

Our recently published study of the ME/CFS patients’ ‘expressed gene profile’ (transcriptome) compared with age/gender matched controls of the Dunedin study suggested the expression of many genes encoding products of biochemical pathways are depressed, complementing the conclusions of a 2016 Stanford University study of plasma metabolites that gave data indirectly suggesting ME/CFS patients have ~20 biochemical pathways functioning at a lower level than normal and are in a ‘state of hibernation’. One way this could happen is if there were a change in the dynamics of the epigenetic code - a DNA code that responds to environmental /nutritional influences – this encompasses DNA methylation, which is a genomic regulatory system linked to changes in gene expression when detected around the on/off switches of genes. We are examining 30 million sites in the DNA genomes of patients in the Dunedin study, and of a second study group of patients undergoing relapse /recovery cycles. This will enable us to deduce which individual genes are affected, and how that translates into lower efficiency of biochemical pathways that might be sustaining ME/CFS.



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