Neuroimmune model
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The neuroimmune model or neuro immune hypothesis of ME/CFS proposes that an initial infection and immune activation, which can be caused by a number of different pathogens results in "a state of chronic peripheral immune activation driven by activated O&NS pathways that lead to progressive damage of self epitopes even when the initial infection has been cleared".[1]
The ATP deficiency, inflammation and oxidative and nitrosative stress are proposed to result from this, and to be the cause of the symptoms characteristic of ME/CFS.[1]
Theory[edit | edit source]
Evidence[edit | edit source]
Treatment[edit | edit source]
Notable studies and publications[edit | edit source]
- 2011, Chronic fatigue syndrome – A neuroimmunological model[2] (Full text)
- 2013, A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome[1] (Full text)
- 2017, The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)[3] (Full text)
See also[edit | edit source]
- O&NS pathway
- Gerwyn Morris
- Michael Maes
- Medical hypotheses (category)
Learn more[edit | edit source]
References[edit | edit source]
- ↑ 1.0 1.1 1.2 Morris, Gerwyn; Maes, Michael (December 2013). "A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome". Metabolic Brain Disease. 28 (4): 523–540. doi:10.1007/s11011-012-9324-8. ISSN 1573-7365. PMID 22718491.
- ↑ Arnett, S.V.; Alleva, L.M.; Korossy-Horwood, R.; Clark, I.A. (July 1, 2011). "Chronic fatigue syndrome – A neuroimmunological model" (PDF). Medical Hypotheses. 77 (1): 77–83. doi:10.1016/j.mehy.2011.03.030. ISSN 0306-9877.
- ↑ Glassford, Julian A.G. (February 17, 2017). "The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)". Frontiers in Physiology. 8. doi:10.3389/fphys.2017.00088. ISSN 1664-042X. PMC 5314655. PMID 28261110.
- ↑ Morris, Gerwyn; Maes, Michael (December 2013). "A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome". Metabolic Brain Disease. 28 (4): 523–540. doi:10.1007/s11011-012-9324-8. ISSN 1573-7365. PMID 22718491.
