La Trobe
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Pathological Mechanisms Underlying Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

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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 a 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 mostly comprised of disturbances to immunological and inflammatory pathways, autonomic and neurological dysfunction, abnormalities in muscle and mitochondrial function, shifts in metabolism, and gut physiology or gut microbiota disturbances. It is possible that these threads are together entangled as parts of an underlying molecular pathology reflecting a far-reaching homeostatic shift. 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.

Funding

D.M. was the recipient of a La Trobe University Postgraduate Scholarship and Australian Government Research Training Program Fees Offset. This work was supported by generous patient donations and grants from the Judith Jane Mason & Harold Stannett Williams Memorial Foundation (Grant IDs: MAS2016F063, MAS2018F00026) and the McCusker Charitable Foundation.

History

Publication Date

01/01/2019

Journal

Diagnostics

Volume

9

Issue

3

Article Number

80

Pagination

20p.

Publisher

MDPI AG

ISSN

2075-4418

Rights Statement

The Author reserves all moral rights over the deposited text and must be credited if any re-use occurs. Documents deposited in OPAL are the Open Access versions of outputs published elsewhere. Changes resulting from the publishing process may therefore not be reflected in this document. The final published version may be obtained via the publisher’s DOI. Please note that additional copyright and access restrictions may apply to the published version.