Mitochondria and immunity in chronic fatigue syndrome

  title={Mitochondria and immunity in chronic fatigue syndrome},
  author={George Anderson and Michael Maes},
  journal={Progress in Neuro-Psychopharmacology and Biological Psychiatry},
  • G. Anderson, M. Maes
  • Published 26 May 2020
  • Biology, Medicine
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry
The Gut Microbiome in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS)
It is suspected that the microbiome may contribute to neurocognitive impairments of ME/CFS patients and the therapeutic potential of fecal microbiota transfer and of targeted dietary interventions should be systematically evaluated.
Lessons From Heat Stroke for Understanding Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
An overview of the pathophysiological mechanisms during heat stroke and similar mechanisms found in myalgic encephalomyelitis/chronic fatigue syndrome are described, which suggest common pathways in the physiological responses to very different forms of stressors, which are manifested in different clinical outcomes.
Animal Models for Neuroinflammation and Potential Treatment Methods
The findings of the included studies suggest that anti-inflammatory substances may be used as effective therapies to ameliorate disease symptoms in patients with ME/CFS.
Perspective: Drawing on Findings From Critical Illness to Explain Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
This paper summarizes and expands on the previous publications about the relevance of findings from critical illness for ME/CFS and describes interlinkages between these pathophysiological mechanisms as well as “vicious cycles” involving cytokines and inflammation that may contribute to explain the chronic nature of these illnesses.
In schizophrenia, chronic fatigue syndrome- and fibromyalgia-like symptoms are driven by breakdown of the paracellular pathway with increased zonulin and immune activation-associated neurotoxicity.
FF symptoms are part of the phenome of schizophrenia and BCPS-worsening as well, and belong to a common core shared by G-CoDe, symtopmatome, and QoL phenomenome.
COVID-19 and post-infectious myalgic encephalomyelitis/chronic fatigue syndrome: a narrative review
There is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS, but there are important similarities between post-acute CO VID-19 symptoms and ME/ CFS.
SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing
The data that might support the idea that mitochondrial health, induced by a healthy lifestyle, could be a key factor in resisting the virus, and for those people who are perhaps not in optimal health, treatments that could support mitochondrial function might be pivotal to their long-term recovery are reviewed.
Effect of Dietary Coenzyme Q10 Plus NADH Supplementation on Fatigue Perception and Health-Related Quality of Life in Individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Prospective, Randomized, Double-Blind, Placebo-Controlled Trial
Overall, the findings support the use of CoQ10 plus NADH supplementation as a potentially safe therapeutic option for reducing perceived cognitive fatigue and improving the health-related quality of life in ME/CFS patients.


Myalgic Encephalomyelitis/Chronic Fatigue Syndrome—Metabolic Disease or Disturbed Homeostasis due to Focal Inflammation in the Hypothalamus?
It is proposed that stimulation of hypothalamic mast cells by environmental, neuroimmune, pathogenic and stress triggers activates microglia, leading to focal inflammation in the brain and disturbed homeostasis, which could be targeted for the development of novel effective treatments.
Chronic fatigue syndrome and the immune system: Where are we now?
Epigenetic modifications and glucocorticoid sensitivity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
Modifications to epigenetic loci associated with differences in glucocorticoid sensitivity may be important as biomarkers for future clinical testing and align with recent ME/CFS work that point towards impairment in cellular energy production in this patient population.
Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?
It is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.
Insights into myalgic encephalomyelitis/chronic fatigue syndrome phenotypes through comprehensive metabolomics
The pathogenesis of ME/CFS, a disease characterized by fatigue, cognitive dysfunction, sleep disturbances, orthostatic intolerance, fever, irritable bowel syndrome (IBS), and lymphadenopathy, is
A systematic review of enteric dysbiosis in chronic fatigue syndrome/myalgic encephalomyelitis
There is currently insufficient evidence for enteric dysbiosis playing a significant role in the pathomechanism of CFS/ME, and Recommendations for future research in this field include the use of consistent criteria for the diagnosis of C FS/ME.
Integrating Pathophysiology in Migraine: Role of the Gut Microbiome and Melatonin.
  • G. Anderson
  • Biology, Psychology
    Current pharmaceutical design
  • 2019
It is proposed that suboptimal mitochondria functioning and metabolic regulation drive alterations in astrocytes and satellite glial cells that underpin the vasoregulatory and nociceptive changes in migraine.
Multiple Sclerosis, Gut Microbiota and Permeability: Role of Tryptophan Catabolites, Depression and the Driving Down of Local Melatonin.
Alterations in the regulation of local melatonergic pathway activation is proposed to be an important hub for such pathophysiological processes in MS, allowing for the increased frequency of depression that may be prodromal in MS to become more intimately associated with the etiology and course of MS.
Myalgic encephalomyelitis/chronic fatigue syndrome patients exhibit altered T cell metabolism and cytokine associations.
Patients with myalgic encephalomyelitis/chronic fatigue syndrome have impaired T cell metabolism consistent with ongoing immune alterations in ME/CFS that may illuminate the mechanism behind this disease.