Otago University (NZ) is fundraising for Prof. Tate's team's ME research

[Ravn]

The University of Otago is currently asking for donations (NZ & International) to support the work of Prof. Tate and his team: https://alumni.otago.ac.nz/donate/myalgic-encephalitis

If you can't contribute financially, maybe you could share the link on your FB, Twitter, etc.

The website above only states that donations are to support research into ME, without any further detail, but Prof Tate has kindly provided some additional information, and permission to share.

Research into ME is not a priority in NZ and funding via the mainstream channels is difficult and uncertain, hence the drive for donations.

Up to now, sometimes I have not known where our money was going to come from to continue the research even a week or two ahead [...] I am very proud of what my small team has achieved on such a small ‘uncertain’ budget.

Despite the funding challenges they have managed to do some interesting work. Two recent publications:

A compromised paraventricular nucleus within a dysfunctional hypothalamus: A novel neuroinflammatory paradigm for ME/CFS
Angus Mackay, Warren P Tate in International Journal of Immunopathology and Pharmacology (Dec 2018) https://doi.org/10.1177/2058738418812342

Changes in the transcriptome of circulating immune cells of a New Zealand cohort with myalgic encephalomyelitis/chronic fatigue syndrome
Eiren Sweetman, Margaret Ryan, Christina Edgar, Angus MacKay, Rosamund Vallings, Warren Tate in International Journal of Immunopathology and Pharmacology (Jan 2019) https://doi.org/10.1177/2058738418820402

This latter study has led to the team now collaborating with Prof Montoya at Stanford on a study on cytokine abnormalities.

Their programme for 2019, for which donations are being sought:

In 2019 the Tate Research group is focussing on ME/CFS patient studies in two important areas of research.
(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. We will also investigate the levels of an important component of this energy production, CoQ10, in plasma and immune cells and whether the status of this biomolecule can be improved by the freely available supplement MitoQ. To assess whether MitoQ as an antioxidant improves energy production in the cells, it will be added to pure immune cells isolated from patients, and as well we will 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.

Our studies groups will include samples taken from (i) our original Dunedin Study patient group, (ii) a new patient group recruited specifically for bioenergetic analyses with our new Seahorse bioanalyser, (iii) patients who have been in a relapse/recovery study group, (iv) A pre- and post exercise study group who have been documented to have experienced post exertional malaise (exercise intolerance) at 24h.

(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 (Sweetman et al., International Journal of Immunopathology and Pharmacology –January 2019) 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. One way this could happen is if there were a change in the dynamics of the epigenetic code – this encompasses the methylation tags on DNA around the on/off switches for the expression 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, using reduced bisulphite sequencing. 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.

I've attached a pdf with some additional responses from Prof. Tate.

I for one will be diverting some of my donation budget their way this year. We can't afford to lose any ME research teams, least of all one containing some young scientists with good brains, judging by their recent papers.