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The neuro-immune pathophysiology of central and peripheral fatigue in systemic immune-inflammatory and neuro-immune diseases

Morris, Gerwyn, Berk, Michael, Galecki, Piotr, Walder, Ken and Maes, Michael 2016, The neuro-immune pathophysiology of central and peripheral fatigue in systemic immune-inflammatory and neuro-immune diseases, Molecular neurobiology, vol. 53, no. 2, pp. 1195-1219, doi: 10.1007/s12035-015-9090-9.

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Title The neuro-immune pathophysiology of central and peripheral fatigue in systemic immune-inflammatory and neuro-immune diseases
Author(s) Morris, Gerwyn
Berk, MichaelORCID iD for Berk, Michael orcid.org/0000-0002-5554-6946
Galecki, Piotr
Walder, KenORCID iD for Walder, Ken orcid.org/0000-0002-6758-4763
Maes, Michael
Journal name Molecular neurobiology
Volume number 53
Issue number 2
Start page 1195
End page 1219
Total pages 25
Publisher Springer
Place of publication Berlin, Germany
Publication date 2016-03
ISSN 1559-1182
Keyword(s) CFS
Chronic fatigue syndrome
Inflammation
Neuroprogression
Oxidative and nitrosative stress
Tryptophan catabolites
Summary Many patients with systemic immune-inflammatory and neuro-inflammatory disorders, including depression, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's disease, cancer, cardiovascular disorder, Parkinson's disease, multiple sclerosis, stroke, and chronic fatigue syndrome/myalgic encephalomyelitis, endure pathological levels of fatigue. The aim of this narrative review is to delineate the wide array of pathways that may underpin the incapacitating fatigue occurring in systemic and neuro-inflammatory disorders. A wide array of immune, inflammatory, oxidative and nitrosative stress (O&NS), bioenergetic, and neurophysiological abnormalities are involved in the etiopathology of these disease states and may underpin the incapacitating fatigue that accompanies these disorders. This range of abnormalities comprises: increased levels of pro-inflammatory cytokines, e.g., interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF) α and interferon (IFN) α; O&NS-induced muscle fatigue; activation of the Toll-Like Receptor Cycle through pathogen-associated (PAMPs) and damage-associated (DAMPs) molecular patterns, including heat shock proteins; altered glutaminergic and dopaminergic neurotransmission; mitochondrial dysfunctions; and O&NS-induced defects in the sodium-potassium pump. Fatigue is also associated with altered activities in specific brain regions and muscle pathology, such as reductions in maximum voluntary muscle force, downregulation of the mitochondrial biogenesis master gene peroxisome proliferator-activated receptor gamma coactivator 1-alpha, a shift to glycolysis and buildup of toxic metabolites within myocytes. As such, both mental and physical fatigue, which frequently accompany immune-inflammatory and neuro-inflammatory disorders, are the consequence of interactions between multiple systemic and central pathways.
Language eng
DOI 10.1007/s12035-015-9090-9
Field of Research 110319 Psychiatry (incl Psychotherapy)
Socio Economic Objective 920410 Mental Health
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2016, Springer
Persistent URL http://hdl.handle.net/10536/DRO/DU:30073850

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
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