Ran into something that may pertain to something I posted earlier. Another way leronlimab can help across a wide range of diseases.
A scientist believes that part of the problem with ME/CFS may be excessive nitrogen. Mitochondria protect cells against Reactive Oxygen and Nitrogen Species.
Then we have mitochondrial dysfunctions effect on neurological disorders.
But it doesn't stop there.
Quote:A possible explanation - Mitochondria are cells that are essential in the conversion of glucose to energy. Excessive damage to mitochondria means less efficient usage of glucose and more storage to fat. a1-antitrypsin is protective of mitochondria.
IL-13 is increased in inflammatory states. IL-13 can significantly decrease amounts of a1-antitrypsin. CCR5 blockade downregulates IL-13 leading to an increase in a1-antitrypsin and protection of mitochondria.
I originally ran into a1-antitrypsin while looking at Covid caused mitochondria damage. What's interesting is that low levels of a1-antitrypsin are also implicated in liver disease and pulmonary inflammation. No one seems to have made the connection between CCR5 blockade, IL-13, a1-antitrypsin and mediation of a variety of diseases.
https://investorshangout.com/post/view?id=6229335
A scientist believes that part of the problem with ME/CFS may be excessive nitrogen. Mitochondria protect cells against Reactive Oxygen and Nitrogen Species.
Quote:Metabolomic studies suggested that people with ME/CFS were using amino acids for fuel at a faster rate than healthy controls.
The metabolomic studies suggest, though, that the nitrogen elimination system in ME/CFS is being overwhelmed – leaving the nitrogen to be eliminated in the form of ammonia (!) (which contains nitrogen) or nitric oxide/peroxynitrite – both of which can be highly toxic.
https://www.healthrising.org/blog/2020/09/24/...akthrough/
Then we have mitochondrial dysfunctions effect on neurological disorders.
Quote:Besides their role in energy production, mitochondria are dynamicorganelles continuously subjected to cycles of fission and fusion. Thus,mitochondria are communicated with each other and also with otherorganelles in order to meet the energetic needs of the cell, as well as toprevent cellular damage caused by excessive RONS, Ca2+influx ormitochondrial DNA mutations.An intact mitochondrial dynamic system is of particular relevancefor neurons. Neurons have a special need to continuously clear cy-tosolic Ca2+and Na+by pumping them out at the expense of large ATPexpenditure, a process that, together with biosynthesis, release and re-uptake of neurotransmitters, is essential for the action potential.
https://www.researchgate.net/publication/2223...plications
But it doesn't stop there.
Quote:In addition to the
physiological processes controlled by mitochondrial ROS, a large body of evidence indicates that mitochondrial oxidative imbalance is responsible for the development and progression of a series of abnormalities such as cancer, diabetes, inflammatory diseases, hypertension, neurodegenerative and ischemia-related diseases, as well as aging
https://www.researchgate.net/profile/Julio-Fe...Health.pdf
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