Jonathan Edwards
Senior Member (Voting Rights)
My thinking is that if it's true that PET markers show activated glia in long covid, as the authors say, and if it's true that activated glia can cause synaptic remodeling, as they also say (I haven't read any of these studies yet), then that seems a decent enough idea for how an infection could cause (maybe temporary) synaptic changes that lead to ME/CFS or other symptoms.
Is there any evidence of activated microglia in Long Covid? I was not aware of that.
I don't think one can start joining dots like this until one can specify precisely where any glia might be activated and why there rather than all over. Encephalitis will activate microglia but general encephalitis produces coma and death. Local encephalitis produces specific localising signs, at least at some sites. In the context of a virus microglia are likely to get activated because of viral infection of cells - which cells and where and what evidence do we have?
These things are possible but theories that repeat fashionable memes without any very specific evidence and without detail on local context are usually dead ends.
And of course synaptic pruning goes on every day in the absence of glial activation - as part of learning from daily experience.