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Pharmacol Res. 2019 Sep 8:104450. doi: 10.1016/j.phrs.2019.104450. [Epub ahead of print]

Myalgic encephalomyelitis/chronic fatigue syndrome: From pathophysiological insights to novel therapeutic opportunities.

Author information

1
IMPACT Strategic Research Centre, School of Medicine, Deakin University, Barwon Health, Geelong, Australia.
2
Department of Medicine, Hammersmith Hospital, Imperial College London, London, UK.
3
Department of Psychiatry, University of Toronto, Toronto, ON, Canada; The Centre for Addiction and Mental Health (CAMH), Toronto, ON, Canada.
4
CMMR Strategic Research Centre, School of Medicine, Deakin University, Geelong, Victoria, Australia.
5
IMPACT Strategic Research Centre, School of Medicine, Deakin University, Barwon Health, Geelong, Australia; CMMR Strategic Research Centre, School of Medicine, Deakin University, Geelong, Victoria, Australia; Orygen, The National Centre of Excellence in Youth Mental Health, Melbourne, Australia.; The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Parkville, Australia; Department of Psychiatry, University of Melbourne, Parkville, Australia.. Electronic address: michael.berk@barwonhealth.org.au.

Abstract

Myalgic encephalomyelitis (ME) or chronic fatigue syndrome (CFS) is a common and disabling condition with a paucity of effective and evidence-based therapies, reflecting a major unmet need. Cognitive behavioural therapy and graded exercise are of modest benefit for only some ME/CFS patients, and many sufferers report aggravation of symptoms of fatigue with exercise. The presence of a multiplicity of pathophysiological abnormalities in at least the subgroup of people with ME/CFS diagnosed with the current international consensus "Fukuda" criteria, points to numerous potential therapeutic targets. Such abnormalities include extensive data showing that at least a subgroup has a pro-inflammatory state, increased oxidative and nitrosative stress, disruption of gut mucosal barriers and mitochondrial dysfunction together with dysregulated bioenergetics. In this paper, these pathways are summarised, and data regarding promising therapeutic options that target these pathways are highlighted; they include coenzyme Q10, melatonin, curcumin, molecular hydrogen and N-acetylcysteine. These data are promising yet preliminary, suggesting hopeful avenues to address this major unmet burden of illness.

KEYWORDS:

Chronic fatigue syndrome; Inflammation; Mitochondrial dysfunction; Myalgic encephalomyelitis; Oxidative stress

PMID:
31509764
DOI:
10.1016/j.phrs.2019.104450

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