berk-centralpathways-2015.pdf (800.36 kB)
Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses
journal contribution
posted on 2015-12-01, 00:00 authored by G Morris, Michael BerkMichael Berk, Ken WalderKen Walder, M. MaesThe 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 MedicineVolume
13Issue
28Pagination
1 - 23Publisher
BioMed CentralLocation
London, Eng.Publisher DOI
eISSN
1741-7015Language
engPublication classification
C Journal article; C1 Refereed article in a scholarly journalCopyright notice
2015, BioMed CentralUsage metrics
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No categories selectedKeywords
Science & TechnologyLife Sciences & BiomedicineMedicine, General & InternalGeneral & Internal MedicineImmuneInflammationOxidative stressToll-like receptorFatigueMitochondriaMultiple sclerosisChronic fatigue syndromeParkinson's diseaseSYSTEMIC-LUPUS-ERYTHEMATOSUSMAJOR DEPRESSIVE DISORDERTOLL-LIKE RECEPTORSPRIMARY SJOGRENS-SYNDROMETUMOR-NECROSIS-FACTORCEREBRAL GLUCOSE-METABOLISMMULTIPLE-SCLEROSIS PATIENTSMITOCHONDRIAL COMPLEX-ICENTRAL-NERVOUS-SYSTEMQUALITY-OF-LIFE
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