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Pathological Mechanisms Underlying Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Sunday 21 July 2019
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Pathological Mechanisms Underlying Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Daniel Missailidis, Sarah Annesley 
, Paul Fisher *
Version 1 : Received: 15 July 2019 / Approved: 16 July 2019 / Online: 16 July 2019 (12:41:26 CEST
© 2019 MDPI (Basel, Switzerland) unless otherwise stated.
Abstract
The underlying molecular basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is not well understood. Characterized by chronic, unexplained fatigue, a disabling payback following exertion (“post-exertional malaise”) and variably presenting, multi-system symptoms, ME/CFS is a complex disease which demands concerted biomedical investigation from disparate fields of expertise.
ME/CFS research and patient treatment have been challenged by the lack of diagnostic biomarkers and finding these is a prominent direction of current work.
Despite these challenges, modern research demonstrates a tangible biomedical basis for the disorder across many body systems.
This evidence is largely comprised of disturbances to immunological and inflammatory pathways, autonomic and neurologic systems, abnormalities in muscle and mitochondrial function, shifts in metabolism, and gut physiology or gut microbiome disturbances.
It is possible that these threads are together entangled as parts of an underlying molecular pathology reflecting a far-reaching homeostatic shift affecting each of these systems.
Due to the variability of non-overlapping symptom presentation or precipitating events such as infection or other bodily stresses, the initiation of body-wide pathological cascades with similar outcomes stemming from different causes may be implicated in the condition.
Patient stratification to account for this heterogeneity is therefore one important consideration during exploration of potential diagnostic developments.
Subject Areas
Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, ME/CFS, diagnosis, metabolism, mitochondria, inflammation, immune system, signaling, gut microbiota.
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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