glial activities

loki

Well-Known Member
so do i get this right? 10% of the brain first-line immune defence consists of microglia cells that have active sensor function and scan their environment radius for infiltration activity, when active they secrete reactive chemicals that destroy infiltration activities which also leads to dysfunction of normal brain chemistry and disruption of chemical balances. is it right that microglia changes its appearance when activated for a long period of time, and then, is sensitive to environmental stimulants which can likely cause a chronic activity loop and they will never leave this state again until they get killed ?
 

weyland

Well-Known Member
More or less, but it's important to note that they also have neuroprotective effects as well (M2 phenotype) and likely contribute to normal functioning of neurons.

[bimg=no-lightbox]http://stroke.ahajournals.org/content/46/Suppl_1/ATP80/embed/graphic-1.gif[/bimg]

What I find interesting is that despite the activated microglia hypothesis making some sense (and the PET evidence for the present of activation markers) the CSF of ME patients is found to be highly deficient in the cytokines that are released by activated microglia (such as IL-1B, IL-6, etc.)
 

loki

Well-Known Member
hm, regarding the abscence of cytokines in CS fluid: maybe because the hallmark of ME / CFS are elevated viral titer and the body will adjust to it with an immune response in the first place, but when the viral population is under control after a strong initial cytokine response, cytokine levels fall and stay at a low concentration. the question for me is wether this initial first cytokine response can alter the microglia in its structure (or appearance), so that it is more sensitive towards signals in the future. That would explain CFS symptoms after an active, intense infection even without any virus titer.
 

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