Marco
Grrrrrrr!
- Messages
- 2,386
- Location
- Near Cognac, France
Sorry I haven't been following this thread but as @Hip tagged me I thought I'd chip in.
I'm still keen on the idea that neuroinflammation/microglial activation plays a central role in ME/CFS. What I've been unsure about is whether this state is self-sustaining (which implies as Jarred Younger suggests that the microglia are responding in an exaggerated manner to normal physiological signals) or if (as appears to be the case with certain types of neuropathic pain) that activated microglia (central sensitisation if you like) needs constant peripheral stimulation (via for example small fibre neuropathy) to sustain it.
I was also keen to find a 'common signal' that might cover all of the 'stressors', from exercise to psychological stress that aggravate symptoms and induce PEM presumably via activated microglia.
One reasonable candidate is something called high mobility group box -1 protein (HMGB1) which appears to be the 'proximal' signal that 'alerts' microglia to everything from peripheral cellular stress to psychological stress.
A deficit in HSP production for example would result in elevated and prolonged cellular stress (oxidative/ER?) which would supply a more of less constant stream of 'danger signals' to already primed microglia.
I'm still keen on the idea that neuroinflammation/microglial activation plays a central role in ME/CFS. What I've been unsure about is whether this state is self-sustaining (which implies as Jarred Younger suggests that the microglia are responding in an exaggerated manner to normal physiological signals) or if (as appears to be the case with certain types of neuropathic pain) that activated microglia (central sensitisation if you like) needs constant peripheral stimulation (via for example small fibre neuropathy) to sustain it.
I was also keen to find a 'common signal' that might cover all of the 'stressors', from exercise to psychological stress that aggravate symptoms and induce PEM presumably via activated microglia.
One reasonable candidate is something called high mobility group box -1 protein (HMGB1) which appears to be the 'proximal' signal that 'alerts' microglia to everything from peripheral cellular stress to psychological stress.
A deficit in HSP production for example would result in elevated and prolonged cellular stress (oxidative/ER?) which would supply a more of less constant stream of 'danger signals' to already primed microglia.
Last edited:
