The ME Association is all in on the mitochondria in ME/CFS. Not only have they been funding or co-funding three other mitochondrial studies, two of them are producing new ways to measure how the mitochondria are doing - a vital need.
A former study may have linked mitochondrial problems to poor immune system functioning - an avenue of research Ron Davis is pursuing. The Lipin/Hornig blood study found that the immune system in longer duration ME/CFS patients appears to be down-regulated. Because innate immune cells are amongst the most active in the body they're a good place to study the mitochondria. The Association's finding that neutrophils have low mitochondrial functioning could provide a reason why.
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Now the Association is funding a project to find out how to directly measure the mitochondria's ability to regenerate ATP, which the association said would greatly improve our ability to assess mitochondrial functioning. (One nice thing about the grant is it's time span - 5 months! No multi-year studies here...)
The Association is also funding a study comparing the efficacy of a blood test developed by Dr. Myhill in relation to other more widely available blood tests.
It's also funding a study examining if the mitochondria in ME/CFS are producing chronic low-level inflammation. I just returned from a talk in which Dr. Naviaux explained that he believes that mitochondrial problems produce inflammation in a wide variety of diseases including ME/CFS. In fact, Naviaux believes the mitochondria may be the primary inflammatory triggers in the body.
It's definitely mitochondria time for ME/CFS; the ME Association, the Chronic Fatigue Initiative and Maureen Hanson, and Robert Naviaux in San Diego and Ron Davis at his Stanford ME/CFS research center are all looking deeply at the mitochondria in ME/CFS. Expect a study from Robert Naviaux that finds mitochondrial problems in ME/CFS to be published soon. (A larger study to validate the results is already underway.)
There is one bit of negative news on the mitochondrial front: Dr. Newton has failed to find any evidence of mitochondrial (or pH or lactate) problems in the muscles of ME/CFS patients.Earlier studies had suggested that pH / lactate problems might play a major role but a followup study did not.
From the ME Association news release:
A former study may have linked mitochondrial problems to poor immune system functioning - an avenue of research Ron Davis is pursuing. The Lipin/Hornig blood study found that the immune system in longer duration ME/CFS patients appears to be down-regulated. Because innate immune cells are amongst the most active in the body they're a good place to study the mitochondria. The Association's finding that neutrophils have low mitochondrial functioning could provide a reason why.
[fright]
Now the Association is funding a project to find out how to directly measure the mitochondria's ability to regenerate ATP, which the association said would greatly improve our ability to assess mitochondrial functioning. (One nice thing about the grant is it's time span - 5 months! No multi-year studies here...)
The Association is also funding a study comparing the efficacy of a blood test developed by Dr. Myhill in relation to other more widely available blood tests.
It's also funding a study examining if the mitochondria in ME/CFS are producing chronic low-level inflammation. I just returned from a talk in which Dr. Naviaux explained that he believes that mitochondrial problems produce inflammation in a wide variety of diseases including ME/CFS. In fact, Naviaux believes the mitochondria may be the primary inflammatory triggers in the body.
It's definitely mitochondria time for ME/CFS; the ME Association, the Chronic Fatigue Initiative and Maureen Hanson, and Robert Naviaux in San Diego and Ron Davis at his Stanford ME/CFS research center are all looking deeply at the mitochondria in ME/CFS. Expect a study from Robert Naviaux that finds mitochondrial problems in ME/CFS to be published soon. (A larger study to validate the results is already underway.)
There is one bit of negative news on the mitochondrial front: Dr. Newton has failed to find any evidence of mitochondrial (or pH or lactate) problems in the muscles of ME/CFS patients.Earlier studies had suggested that pH / lactate problems might play a major role but a followup study did not.
From the ME Association news release:
Over the last 20-30 years, attempts by researchers using techniques successfully applied to identify mitochondrial defects in patients with genetic defects in the mitochondrial respiratory chain have consistently failed to identify mitochondrial abnormalities in CFS/ME patients.
Between, 2009-2013 a series of papers by Booth/Myhill et al [2-4] have demonstrated an interesting correlation between the level of mitochondrial dysfunction in a specific type of white blood cell called a neutrophil and the severity of disease in ME/CFS patients.
In addition to measuring total cellular energy in the form of a chemical called adenosine triphosphate (ATP) the authors use novel approaches to measure the ability of mitochondria to regenerate ATP following depletion of mitochondria ATP with the electron transfer chain (ETC) inhibitor sodium azide.
Such an approach is claimed to be a major advance on current approaches which just measure steady state levels of ATP and adenosine diphosphate (ADP) in isolated organelles or whole cells.
As steady state ATP levels are a consequence of supply and demand they do not always reflect the ability of mitochondria to generate ATP.
MEA project grant (5 months):
Establishing protocols to assess mitochondrial function in Neutrophils and Monocytes from ME/CFS patients.
The current pilot study is to set up the tests required to assess mitochondrial function in blood samples from ME/CFS patients.
For this we will use cell models with known mitochondrial dysfunction and bio-energetic impairment to both validate and improve on the tests developed by Acumen [2-4].
Our goal is to develop a method to assess mitochondrial function compatible with the widely used Seahorse Biosciences metabolic flux analyzer and plate based fluorescent probe oxygen and pH measuring platforms.
This will make the blood tests more globally accessible to a wide range of researchers allowing a more universal validation of the findings of Booth/Myhill.
Other MEA RRF research involving mitochondria in ME/CFS.
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