Abstract | BACKGROUND: DISCUSSION: Multiple lines of evidence demonstrate a positive association between the degree of peripheral immune activation, inflammation and oxidative stress, gray matter atrophy, glucose hypometabolism and cerebral hypoperfusion in illness, such as multiple sclerosis, Parkinson's disease and chronic fatigue syndrome. Most, if not all, of these abnormalities can be explained by a reduction in the numbers and function of astrocytes secondary to peripheral immune activation and inflammation. This is also true of the widespread mitochondrial dysfunction seen in otherwise normal tissue in neuroinflammatory, neurodegenerative and autoimmune diseases and in many patients with disabling, apparently idiopathic, fatigue. Given the strong association between peripheral immune activation and neuroinflammation with the genesis of fatigue the latter group of patients should be examined using FLAIR magnetic resonance imaging (MRI) and tested for the presence of peripheral immune activation. SUMMARY: It is concluded that peripheral inflammation and immune activation, together with the subsequent activation of glial cells and mitochondrial damage, likely account for the severe levels of intractable fatigue and disability seen in many patients with neuroimmune and autoimmune diseases.This would also appear to be the case for many patients afforded a diagnosis of Chronic Fatigue Syndrome.
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Authors | Gerwyn Morris, Michael Berk, Ken Walder, Michael Maes |
Journal | BMC medicine
(BMC Med)
Vol. 13
Pg. 28
(Feb 06 2015)
ISSN: 1741-7015 [Electronic] England |
PMID | 25856766
(Publication Type: Journal Article, Review)
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Chemical References |
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Topics |
- Autoimmune Diseases
(complications, immunology)
- Cytokines
(immunology)
- Fatigue Syndrome, Chronic
(immunology)
- Humans
- Inflammation
(complications, immunology)
- Neuroimmunomodulation
(immunology)
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