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Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses

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journal contribution
posted on 2015-12-01, 00:00 authored by G Morris, Michael BerkMichael Berk, Ken WalderKen Walder, M. Maes
The genesis of severe fatigue and disability in people following acute pathogen invasion involves the activation of Toll-like receptors followed by the upregulation of proinflammatory cytokines and the activation of microglia and astrocytes. Many patients suffering from neuroinflammatory and autoimmune diseases, such as multiple sclerosis, Parkinson's disease and systemic lupus erythematosus, also commonly suffer from severe disabling fatigue. Such patients also present with chronic peripheral immune activation and systemic inflammation in the guise of elevated proinflammtory cytokines, oxidative stress and activated Toll-like receptors. This is also true of many patients presenting with severe, apparently idiopathic, fatigue accompanied by profound levels of physical and cognitive disability often afforded the non-specific diagnosis of chronic fatigue syndrome.

History

Journal

BMC Medicine

Volume

13

Issue

28

Pagination

1 - 23

Publisher

BioMed Central

Location

London, Eng.

eISSN

1741-7015

Language

eng

Publication classification

C Journal article; C1 Refereed article in a scholarly journal

Copyright notice

2015, BioMed Central