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Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome.

Discussion in 'Latest ME/CFS Research' started by Murph, Dec 8, 2018.

  1. Murph

    Murph :)

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    Front Psychiatry. 2018 Nov 16;9:589. doi: 10.3389/fpsyt.2018.00589. eCollection 2018.
    Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome.
    Noda M1, Ifuku M2, Hossain MS2, Katafuchi T2.
    Author information
    Abstract

    Fatigue is commonly reported in a variety of illnesses and has major impact on quality of life. Chronic fatigue syndrome (CFS) is a debilitating syndrome of unknown etiology. The clinical symptoms include problems in neuroendocrine, autonomic, and immune systems. It is becoming clear that the brain is the central regulator of CFS. For example, neuroinflammation, especially induced by activation of microglia and astrocytes, may play a prominent role in the development of CFS, though little is known about molecular mechanisms. Many possible causes of CFS have been proposed.

    However, in this mini-review, we summarize evidence for a role for microglia and astrocytes in the onset and the maintenance of immunologically induced CFS. In a model using virus mimicking synthetic double-stranded RNA, infection causes sequential signaling such as increased blood brain barrier (BBB) permeability, microglia/macrophage activation through Toll-like receptor 3 (TLR3) signaling, secretion of IL-1β, upregulation of the serotonin transporter (5-HTT) in astrocytes, reducing extracellular serotonin (5-HT) levels and hence reduced activation of 5-HT1A receptor subtype. Hopefully, drug discovery targeting these pathways may be effective for CFS therapy.

    KEYWORDS:
    IL-1beta; TLR3; chronic fatigue syndrome; poly I:C; serotonin transporter

    PMID:
    30505285
    PMCID:
    PMC6250825
    DOI:
    10.3389/fpsyt.2018.00589
     
  2. Research 1st

    Research 1st Severe ME, POTS & MCAS.

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    Interesting paper, thanks for sharing.

    If our BBB is impaired, then our brains run the risk of being slammed by events people without our condition can shrug off.

    E.g. We can end up trashed by a virus that others brush off and return to work. Yet we can report huge increase in brainfog, headache, light and noise sensitivity and vertigo and pain for weeks or months or even years.

    To me, this is an abnormal neuro inflammatory CNS response to something as innocent as a common cold that an autoimmune process switches on/off.

    So are these pathogens, proteins, lymphocytes literally climbing into our brains? Hopefully we'll find out.

    I'm sure the inflammation causes the neuro psych symptoms too, like anxiety and panic disorder many of us are plagued by, post onset, that we never had when healthy
     

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