NIH: Accelerating Research on ME/CFS meeting, 4th and 5th April 2019

Elzakker: “Neuroinflammation” is imprecise, “microglial activation” is a proxy

ETA: Apparently both Younger and Van Elzakker are aware of the issues with the vague language around neuroinflammation, a good sign that they are addressing it.
 
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andypants said:
Elzakker: “Neuroinflammation” is imprecise, “microglial activation” is a proxy

ETA: Apparently both Younger and Van Elzakker are aware of the issues with the vague language around neuroinflammation, a good sign that they are addressing it.
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OK but what is microglial activation a proxy for? And why is it just a proxy rather than important in its own right? If microglial activation is just a bystander then we seem to be chasing even less inflammation.

If microglial activation occurs in the absence of other aspects of inflammation ( vascular changes or cell migration) it may be a response to something non-inflammatory like neuron death or degeneration.

I would like to get away from proxies for invisible snarks amd stick to data and mechanisms.

I may be a grumpy old crust but I don't think these guys are doing themselves justice. Real science answers are REAL; they don't need gilding with excuses. What's more they are there to be found if you look. And they aren't what you are expecting - at least not until you finally seehow it works (unexpectedly).
 
Jonathan Edwards said:
OK but what is microglial activation a proxy for? And why is it just a proxy rather than important in its own right? If microglial activation is just a bystander then we seem to be chasing even less inflammation.

If microglial activation occurs in the absence of other aspects of inflammation ( vascular changes or cell migration) it may be a response to something non-inflammatory like neuron death or degeneration.

I would like to get away from proxies for invisible snarks amd stick to data and mechanisms.

I may be a grumpy old crust but I don't think these guys are doing themselves justice. Real science answers are REAL; they don't need gilding with excuses. What's more they are there to be found if you look. And they aren't what you are expecting - at least not until you finally seehow it works (unexpectedly).
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I'm sure you're right! He said A LOT more but he's talking very fast and to be honest I'm starting to fog over too much to follow. I picked a couple of lines from one of his slides as an example. Just wanted to comment that they are addressing it in some way. Hopefully this will all be posted online so people can take it in in more detail. He was very clear that we can't tell if any of this is particular to ME either, this stuff (whatever it is) is going on in a lot of diseases.

ETA: I think it's great that you are so critical, it can be hard to know what to believe sometimes, especially when processing power ~ 0.

ETA2: I think (just my understanding and vague recollection) that he used 'proxy' because in reality the field is not advanced enough to really be completely sure what they are measuring.
 
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(I haven't been able to follow all of the presentations because of caregiving responsibilities.)
What sort of discussion has taken place during this conference about cognitive problems in ME?
 
Jonathan Edwards said:
something non-inflammatory like neuron death or degeneration
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Aren't there multiple observations of increased... can't remember the right word... cell death (apoptosis?)? Which seems to fit well with observations of decreased telomeres if the cell replacement cycle has to replace cells more than usual.

Do we know what else happens to the cells put in ME plasma (or serum, I think Davis is with plasma and there's another presentation today finding changes with serum?) besides the weird impedance signal? Do they also die quicker or just mostly crap out on energy production but otherwise continue otherwise merrily functioning badly with the same lifespan?
 
If there "something in the blood," I wonder if that might be related to why patients feel better following an infusion - i.e. the blood becomes more dilute, possibly reducing the concentration of "x" to below some kind of symptomatic threshold.

Similarly, if patients have low blood volume, then the concentration of "x" may go up if it is entering the bloodstream at a constant rate unrelated to blood volume.
 
ukxmrv said:
Oh dear. The end roundup is depressing. The concentration so far on Sickness Behaviour
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Always low expectations for Komaroff, who is editor for UpToDate's improved but still-awful CFS section. UpToDate still hasn't completely rejected PACE, and states GET and CBT are beneficial for some ME/CFS patients.

2 decades ago, Komaroff did a presentation for the Medical Board of California where he recommended GET and CBT . He's never corrected this, to the best of my knowledge. It's still on the Medical Board of California website.

Edit: supportive links if anyone is interested
https://www.s4me.info/threads/uptodate-me-cfs-information.5755/
https://www.s4me.info/threads/my-le...still-recommending-get.2085/page-4#post-49180
 
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