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Cited by 117Fibromyalgia and Chronic Fatigue Syndrome ResearchLong-Term Effects of COVID-19Tryptophan and brain disorders

The DOI matches its Crossref record; 207 of the 207 references it cites were found in a registry or an index.

A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome

Morris, Gerwyn, Maes, Michael·2013·Metabolic Brain Disease
DOI 10.1007/s11011-012-9324-8
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Abstract

This paper proposes a neuro-immune model for Myalgic Encephalomyelitis/Chronic fatigue syndrome (ME/CFS). A wide range of immunological and neurological abnormalities have been reported in people suffering from ME/CFS. They include abnormalities in proinflammatory cytokines, raised production of nuclear factor-κB, mitochondrial dysfunctions, autoimmune responses, autonomic disturbances and brain pathology. Raised levels of oxidative and nitrosative stress (O&NS), together with reduced levels of antioxidants are indicative of an immuno-inflammatory pathology. A number of different pathogens have been reported either as triggering or maintaining factors. Our model proposes that initial infection and immune activation caused by a number of possible pathogens leads to 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. Subsequent activation of autoreactive T cells conspiring with O&NS pathways cause further damage and provoke chronic activation of immuno-inflammatory pathways. The subsequent upregulation of proinflammatory compounds may activate microglia via the vagus nerve. Elevated proinflammatory cytokines together with raised O&NS conspire to produce mitochondrial damage. The subsequent ATP deficit together with inflammation and O&NS are responsible for the landmark symptoms of ME/CFS, including post-exertional malaise. Raised levels of O&NS subsequently cause progressive elevation of autoimmune activity facilitated by molecular mimicry, bystander activation or epitope spreading. These processes provoke central nervous system (CNS) activation in an attempt to restore immune homeostatsis. This model proposes that the antagonistic activities of the CNS response to peripheral inflammation, O&NS and chronic immune activation are responsible for the remitting-relapsing nature of ME/CFS. Leads for future research are suggested based on this neuro-immune model.

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Crossref · 10.1007/s11011-012-9324-8

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207 of 207 references verified0 citation errors · 0 not checkable

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Research works printed but not linked: 1

  1. Pincus S (2005) Potential role of infections in chronic inflammatory diseases. ASM News 71:529–535

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Metadata

Authors
Morris, G., & Maes, M.
Affiliations
Piyavate Hospital (TH)
Corresponding author
Maes, Michael
ORCID
Venue
Metabolic Brain Disease
Publisher
Springer Science and Business Media LLC
Published
2012-06-21
Volume
28
Issue
4
Pages
523-540
ISSN
  • 0885-7490 (ISSN-L)
  • 1573-7365
DOI
10.1007/s11011-012-9324-8
OpenAlex
W2035315327
Cited by
117
References
207
Citations by year
2026: 5 · 2025: 5 · 2024: 9 · 2023: 6 · 2022: 8 · 2021: 7 · 2020: 1 · 2019: 11 · 2018: 7 · 2017: 5 · 2016: 14 · 2015: 16 · 2014: 9 · 2013: 14
FWCI
1.68
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Metabolic Brain Disease (publishedVersion)
  • PubMed (publishedVersion)
Funders
World Health Organization
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
  • Health Sciences › Medicine › Clinical Neurology › Long-Term Effects of COVID-19
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
chronic fatigue syndrome, inflammatory cytokines, NF-κB, mitochondrial dysfunction, autoreactive T cells, autoimmunity, molecular mimicry, bystander activation, epitope spreading, microglial activation, vagus nerve, post-exertional malaise, immune activation
MeSH terms
Brain, Fatigue, Humans, Inflammation, Models, Biological, Fatigue Syndrome, Chronic, Cytokines, Oxidative Stress

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