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Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and mitochondria: A review, 2022, Pandey (M.Sc. Thesis)

Discussion in 'ME/CFS research' started by Tom Kindlon, Sep 20, 2022.

  1. Tom Kindlon

    Tom Kindlon Senior Member (Voting Rights)

    Messages:
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    via
    Dr. Marc-Alexander Fluks

    Source: Cornell University Date: May 2022 URL: https://ecommons.cornell.edu/handle/1813/111644

    https://ecommons.cornell.edu/bitstream/handle/1813/111644/Pandey_cornell_0058O_11430.pdf

    Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and mitochondria: A review -----------------------------------------------------------------------------
    Aakarsha Ajit Pandey - Biochemistry, Molecular and Cell Biology, Cornell University, USA

    Abstract

    Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) is a debilitating disorder that affects about 60 million people worldwide and manifests commonly in the aftermath of a viral infection. Symptoms affect immune function, sleep patterns, and cognition and leave patients severely fatigued after normal or less than normal exertion. Mitochondria are responsible for energy metabolism, cell signaling, and oxidative stress pathways in majority of the tissues in the body. Presented here is a review of studies investigating the role of mitochondrial DNA mutations and oxidative phosphorylation output in immune cells and skeletal muscle cells. Also included are studies that are broad metabolomic investigations of blood plasma of ME/CFS patients, and studies that measure markers of oxidative stress. Immune dysfunction emerges to be playing a key role in ME/CFS pathophysiology as well as oxidative stress. Ultimately the interdependence of these processes with the mitochondria at the center starts to paint a clearer picture of the mechanisms at play in this disease.

    Keywords: ME/CFS, OXPHOS, oxidative stress, mtDNA, PBMCs, free radicals

    -------- (c) 2022 Cornell University

    graphical abstract.PNG
     
    Jacob Richter, Hutan, RedFox and 4 others like this.
  2. Creekside

    Creekside Senior Member (Voting Rights)

    Messages:
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    Their graphic is just vague speculation. How does that "start to paint a clearer picture"? Until they can find a clear difference in mitochondrial function in all PWME, it's still just a wild guess as to what the mechanism of ME is. Mitochondrial function is probably involved, but cause or just effect?
     
  3. Mithriel

    Mithriel Senior Member (Voting Rights)

    Messages:
    2,815
    I don't think matters at this point whether it is cause or effect. The important thing is that ME is not a disease of fatigue, which is incidental like calling heart failure a disease of fatigue. It is a disease characterized by a failure to produce enough energy.

    It may be that not being able to produce enough energy is the reason why a virus can remain in the body or a virus may cause damage or a genetic failure causes both but there are enough clues out there to say categorically that energy production systems are involved.

    It is the final nail in the behavioural theories and needs to be proclaimed loudly even if we do not know the exact mechanisms.
     
    Amw66 and Peter Trewhitt like this.

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