The pathobiology of myalgic encephalomyelitis/chronic fatigue syndrome: The case for neuroglial failure

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dc.contributor.authorRenz-Polster, Herbert
dc.contributor.authorTremblay, Marie-Ève
dc.contributor.authorBienzle, Dorothee
dc.contributor.authorFischer, Joachim E.
dc.date.accessioned2024-02-02T19:54:13Z
dc.date.available2024-02-02T19:54:13Z
dc.date.copyright2022en_US
dc.date.issued2022
dc.descriptionWe acknowledge with gratitude the many and intense discussions about the pathobiological basis of ME/CFS on Twitter, to which innumerable experts, researchers, organizations, and – not to forget – patients contribute.en_US
dc.description.abstractAlthough myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) has a specific and distinctive profile of clinical features, the disease remains an enigma because causal explanation of the pathobiological matrix is lacking. Several potential disease mechanisms have been identified, including immune abnormalities, inflammatory activation, mitochondrial alterations, endothelial and muscular disturbances, cardiovascular anomalies, and dysfunction of the peripheral and central nervous systems. Yet, it remains unclear whether and how these pathways may be related and orchestrated. Here we explore the hypothesis that a common denominator of the pathobiological processes in ME/CFS may be central nervous system dysfunction due to impaired or pathologically reactive neuroglia (astrocytes, microglia and oligodendrocytes). We will test this hypothesis by reviewing, in reference to the current literature, the two most salient and widely accepted features of ME/CFS, and by investigating how these might be linked to dysfunctional neuroglia. From this review we conclude that the multifaceted pathobiology of ME/CFS may be attributable in a unifying manner to neuroglial dysfunction. Because the two key features – post exertional malaise and decreased cerebral blood flow – are also recognized in a subset of patients with post-acute sequelae COVID, we suggest that our findings may also be pertinent to this entity.en_US
dc.description.reviewstatusRevieweden_US
dc.description.scholarlevelFacultyen_US
dc.description.sponsorshipFor the publication fee we acknowledge financial support by Deutsche Forschungsgemeinschaft within the funding program “Open Access Publikationskosten” as well as by Heidelberg University. M-ET holds a Tier 2 Canada Research Chair in Neurobiology of Aging and Cognition. DB holds a University Research Chair in Veterinary Pathology.en_US
dc.identifier.citationRenz-Polster, H., Tremblay, M-E., Bienzle, D., & Fischer, J. E. (2022). The pathobiology of myalgic encephalomyelitis/chronic fatigue syndrome: The case for neuroglial failure. Frontiers in Cellular Neuroscience, 16, 888232. https://doi.org/10.3389/fncel.2022.888232en_US
dc.identifier.urihttps://doi.org/10.3389/fncel.2022.888232
dc.identifier.urihttp://hdl.handle.net/1828/15921
dc.language.isoenen_US
dc.publisherFrontiers in Cellular Neuroscienceen_US
dc.subjectchronic fatigue syndrome
dc.subjectmyalgic encephalomyelitis
dc.subjectneuroinflammation
dc.subjectglia
dc.subjectmicroglia
dc.subjectastrocytes
dc.subjectoligodendrocytes
dc.subjectblood brain barrier
dc.subjectCentre for Advanced Materials and Related Technology (CAMTEC)
dc.subject.departmentDivision of Medical Sciences
dc.subject.departmentSchool of Medical Sciences
dc.titleThe pathobiology of myalgic encephalomyelitis/chronic fatigue syndrome: The case for neuroglial failureen_US
dc.typeArticleen_US

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