Dr Karl Morten - UK researcher based at Oxford University

Solstice said:
How do they get any research of the ground then? I might be sounding very ignorant, but if you don't look for clues how are you even starting to put the puzzle together for many diseases?
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I wouldn't worry, this is all grant body political talk. In real science you work in all sorts of ways - according to the needs at the time, and the grant bodies know this and will fund exploratory studies if they think they are appropriate.

The grant bodies say they do not like fishing exercises when they see someone fishing in a pond that nobody found any fish in for the last generation. It gives them a reason to say no when they are not impressed. Grant bodies are run by people who have a pretty poor track record for getting things right but not fishing in an empty pond is not such a bad reason as they go.

All this sort of talk is going round and round in circles. All that really matters is whether a project has a reasonable chance of getting somewhere. And very often that only becomes clear with time.
 
Jonathan Edwards said:
In real science you work in all sorts of ways - according to the needs at the time, and the grant bodies know this and will fund exploratory studies if they think they are appropriate.
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I'd guessed it's probably not entirely different to arts funding. There are Funding Priorities and there is Work You Want To Do, and despite them looking very different it's perfectly possible to make the twain meet. A lot of it is about the way you present your case.
 
Merged thread

Oxford talk: The importance of chronic Infections in chronic disease and the potential role of mitochondria - Morton

Audience: Members of the University only

Date: 20 June 2023, 13:00

  • Speaker: Professor Karl Morten (Nuffield Department of Women's and Reproductive Health, University of Oxford)


    Abstract:
    Mitochondrial therapeutics is an emerging field in medicine with a growing interest from the pharmaceutical sector. Many well know conditions, including Alzheimer’s/Parkinson’s disease, multiple sclerosis and diabetes show mitochondrial dysfunction, which has yet to be fully explored as a potential therapeutic target.

    Other less well-defined chronic conditions, including Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS), Long Covid and Gulf War Syndrome (GWS), also show elements of mitochondrial dysfunction. ME/CFS is the best studied with evidence of energy dysregulation observed in peripheral blood mononuclear cells and a systemic effect with reduced levels of amino acids in plasma possibly linked to alter fuel use.

    Although it is unclear if mitochondrial dysfunction is directly involved in ME/CFS, there appears to be an abnormal energy balance. Patient’s symptoms will worsening if they expend too much energy during physical exertion or undertaking cognitive tasks. Post exertional malaise (PEM) in ME/CFS and Long Covid is a characteristic feature, which differentiates the conditions from clinical depression, which can also associate with severe fatigue.
    Mitochondria are the primary generators of aerobic energy production in eukaryotic tissues, but also have roles in infection, being a key component of the innate immune response to bacterial and viral pathogens, and also dealing with intracellular pathogens. How cells balance the energy and metabolic needs of the cell with other mitochondrial pathogen-associated roles is likely important in the chronic diseases outlined earlier.

    Most of the conditions outlined above are associated with pathogens at some stage of the disease process. Mammalian tissues differ in their mitochondrial content. Heart has the highest number of mitochondria relative to its volume at 37%, while the brain has very few at 5%. With the brain being the largest consumer of oxygen and glucose in the body: how does the brain generate enough energy to meet its high ATP requirement with so few mitochondria? In this presentation, we speculate that in cells with a high aerobic ATP production need other membrane systems containing mitochondrial components are the primary generators of aerobic ATP.

    These membrane systems include myelin in neurons, the membranes of the outer segment of Rod cells in the retina and the endoplasmic reticulum in antibody producing plasmablast cell. All of these cells have a very large aerobic energy need but appear to have insufficient mitochondria. This lack of mitochondria may also impact on the ability of these cell to deal with intracellular pathogens.

    Both mitochondrial DNA shedding to trigger an innate immune response and engulfment of intracellular pathogens both play a role in how we deal with pathogens. With the microbiome, now extending beyond the gut and into our cells and tissues how we work with these invaders is an important factor in our health and well-being. With mitochondria having a significant pathogen defence role, cells lacking mitochondria in the long-term maybe more vulnerable to the establishment of chronic conditions, with genetic and physiological differences in individuals making some more susceptible than others.

    https://talks.ox.ac.uk/talks/id/fa5add0c-410b-429a-8b57-0c64c361333b/
 
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I wonder how match funding works in research?

I'm only familiar with a system of favours, where small companies negotiate bits of spare capacity—rehearsal room days, time in the metalwork shop, loan of equipment that would otherwise be on a shelf—from bigger ones, in return for a reduced show fee.

The small company puts the market value of the favour into their grant application as match funding, and does the cheap show as a first night preview they were never expecting to earn a fee for anyway. The big company blathers on in their grant report about how much support they give the wider arts ecology, and reports a cracking good box office % against fee on that show. Everybody's happy.

You'd think there'd be some of that going on in labs, too?
 
The next MitOx event will take place April 12th 2024. Organised by Karl, this was described last year as an "annual meeting packed with short talks and posters on cancer metabolism, neuroscience, diabetes, mitochondrial disorders and general mitochondrial biology. This one day hybrid conference is ideal for researchers with an interest in mitochondria from both academia and pharma.". ME/CFS is frequently featured.

More details to follow.
 

How does one obtain a Chronic Lyme (I'm assuming that this is equivalent to Post-Treatment Lyme Disease Syndrome) cohort? Isn't the diagnosis typically made on the basis of tests that are highly unreliable? Are there serious researchers in the field that have also established rigorous cohorts (I'm not questioning Chronic Lyme, I'm just wandering how robust a cohort would be)?
 
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