Shared microglial mechanisms underpinning depression and chronic fatigue syndrome and their comorbidities. (Chaves-Filho, 2019)

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Behav Brain Res. 2019 Oct 17;372:111975. doi: 10.1016/j.bbr.2019.111975. Epub 2019 May 25.
Shared microglial mechanisms underpinning depression and chronic fatigue syndrome and their comorbidities.
Chaves-Filho AJM1, Macedo DS2, de Lucena DF3, Maes M4.
Author information
1Neuropsychopharmacology Laboratory, Drug Research and Development Center, Faculty of Medicine, Federal University of Ceara, Fortaleza, CE, Brazil. Electronic address: adrianoafilho@hotmail.com.
2Neuropsychopharmacology Laboratory, Drug Research and Development Center, Faculty of Medicine, Federal University of Ceara, Fortaleza, CE, Brazil; National Institute for Translational Medicine (INCT-TM, CNPq), Ribeirão Preto, Brazil. Electronic address: daniellesilmacedo@gmail.com.
3Neuropsychopharmacology Laboratory, Drug Research and Development Center, Faculty of Medicine, Federal University of Ceara, Fortaleza, CE, Brazil. Electronic address: daviddelucena@me.com.
4Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; IMPACT Strategic Research Center, Deakin University, Geelong, Australia. Electronic address: dr.michaelmaes@hotmail.com.
Abstract
In 2011, it was reviewed that a) there is a strong co-occurrence between major depression and chronic fatigue syndrome (CFS), with fatigue and physio-somatic symptoms being key symptoms of depression, and depressive symptoms appearing during the course of CFS; and b) the comorbidity between both disorders may in part be explained by activated immune-inflammatory pathways, including increased translocation of Gram-negative bacteria and increased levels of pro-inflammatory cytokines, such as interleukin (IL)-1.

Nevertheless, the possible involvement of activated microglia in this comorbidity has remained unclear. This paper aims to review microglial disturbances in major depression, CFS and their comorbidity. A comprehensive literature search was conducted using the PubMed / MEDLINE database to identify studies, which are relevant to this current review. Depressed patients present neuroinflammatory alterations, probably related to microglial activation, while animal models show that a microglial response to immune challenges including lipopolysaccharides is accompanied by depressive-like behaviors.

Recent evidence from preclinical studies indicates that activated microglia have a key role in the onset of fatigue. In chronic inflammatory conditions, such as infections and senescence, microglia orchestrate an inflammatory microenvironment thereby causing fatigue. In conclusion, based on our review we may posit that shared immune-inflammatory pathways and especially activated microglia underpin comorbid depression and CFS. As such, microglial activation and neuro-inflammation may be promising targets to treat the overlapping manifestations of both depression and CFS.
Copyright © 2019 Elsevier B.V. All rights reserved.
KEYWORDS:
Chronic fatigue syndrome; Cytokines; Major depressive disorder; Microglia; Neuro-immune; Oxidative stress
PMID: 31136774 DOI: 10.1016/j.bbr.2019.111975
 

percyval577

geometrical disaster
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... and perhaps an unwelcome link to depression, ...
If read with care, I think even Per Fink could be right when he says that some - so far (right, Mr Fink?) - unexplained syndromes "may" have "the same underlying phenotype" (Fink 2017).

A good candidate might be certain nerve structures which could be vulnerable to physiological impacts, and I think basal ganglia and thalamus are best candidates. (And b/c the thalamus projects bidirectional to the cortex, there is nothing implicated in any psycho manner.)

The differences seen among such difficult to spot diseases might be in its core "only" a geometrical difference of synaptical patterns of the same pool of nerves.

In so far there might be a core cure possible (probabaly surrounded by other influences) which would be the same as well.