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A neuro-immune explanation for the remitting/relapsing nature of ME/CFS

  [ 155 votes ]   [ 1 Comment ] • June 22, 2012

A neuro-immune model of Myalgic Encephalomyelitis / Chronic fatigue syndrome
– Source: Metabolic Brain Disease, Jun 21, 2012

By Gerwyn Morris, Michael Maes

[Note: Reportedly this model was developed by Gerwyn Morris. Readers may not be as familiar with Morris' work as with that of co-author Michael Maes, whose investigations relating to aspects of this model span more than 25 years. To access a database with links to abstracts of Maes' 120-plus journal articles on the subjects of psycho-neuro-immunology, depression, chronic fatigue, inflammation, cytokines, oxidative stress, mitochondrial function and more, go to]

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-kB,
- 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 [acting against 'self'] 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 [cells in the brain and spinal cord] 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.

Source: Metabolic Brain Disease, Jun 21, 2012. PMID: 22718491, Morris G, Maes M. Tir Na Nog, Pembrey, Llanelli, UK; Maes Clinics@TRIA, Piyavate Hospital, Bangkok, Thailand. [e-mail: Michael Maes, Article currently provides no email contact for Gerwyn Morris.]

* Note: According to

Oxidative stress is “A condition which occurs when the production of free radicals in the human body exceeds the body's ability to neutralize and eliminate them. Oxidative stress can result from a lack of antioxidants or from an over abundance free radicals. Exercise can increase levels of free radicals, increasing the risk of oxidative stress. Free radicals can react with key components of cells, including DNA, lipids, and protein, resulting in cellular damage.

Nitrostative stress is “A condition that occurs when the production of highly reactive nitrogen-containing chemicals such a nitrous oxide exceed the body’s ability to neutralize and eliminate them. Nitrosative stress can lead to reactions that alter protein structure thus interfering with normal body functions."

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Article Comments Post a Comment

The model is the original work of G Morris
Posted by: BandanQ
Jun 22, 2012
The information in your post is incorrect. G Morris is the lead author of the paper and it is his original model.

You can either contact Morris or Maes, otherwise you should change the information.
Reply Reply
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