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Jonathan Edwards said:
I don't think that is realistic, to be honest. The 'inflammatory markers' posted are obscure proteins not normally used as markers. For peripheral inflammation to inhibit TSPO going in to brain I think one would at least want raised C-reactive protein and other acute phase proteins. I would be a bit sceptical even then. (And of course there is no clinical evidence of peripheral inflammation.) I am not sure how it would relate to schizophrenia or depression, either?
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Per the paper @Murph posted and some others I skimmed, I get the impression that there are some proteins typically upregulated during inflammatory conditions that also bind TSPO. The possibility I’m interested in is that some of these proteins remain upregulated somewhere in the periphery in absence of a full inflammatory response. Most “inflammation-associated” genes have binding sites for multiple cytokine-associated transcription factors (NFkB, all the STATs, CREB, ATFs, etc.)—it takes the full concert to induce peak transcription, but even just one or two of those TFs can noticeably upregulate the gene.

To me it’s the explanation that makes the most sense with the increased signal in the some bones and muscle groups that were highlighted. If that peripheral protein sequestering TSPO could be identified it would be a clue towards the upstream signaling abnormality. Especially if the same upstream signaling pathway also happens to induce upregulation of some lipid pathways in B cells, per the @DMissa findings
 
jnmaciuch said:
To me it’s the explanation that makes the most sense with the increased signal in the some bones and muscle groups that were highlighted.
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For me the explanation that makes most sense is that the data don't mean that much - other than being negative for brain inflammation. I am not sure that there are good controls for body uptake. Uptake in marrow might be what you get when everywhere else is not interested.

I agree that there is a faint possibility of something going on in marrow and muscle - and worth someone pursuing. I think that impacting BBB is pretty implausible though.
 
Jonathan Edwards said:
Uptake in marrow might be what you get when everywhere else is not interested.
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Perhaps, but if that was the case we should be seeing only random variation in all the areas measured on the full body scan compared to the healthy controls, who also don’t have anything interesting going on. Instead there was a trend of signal being higher in ME/CFS in all muscle groups and bone marrow tested (reaching significance in several), but [edit: near identical levels or lower in all organs].

Could still be a confounder, maybe that’s what happens when someone spends more time sitting. All in all the pieces point to something potentially interesting though.

Jonathan Edwards said:
The 'inflammatory markers' posted are obscure proteins not normally used as markers.
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agree. Though, interestingly, I can tell you off the top of my head that at least 4 of these are known NFkB/RELA target genes. All of them might be but I’d have to double check
 
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Sean said:
Most signal is found in the shoulders, postural muscles, the neck,...​

Now that is interesting. It fits my experience of pain distribution.

Also might help explain sleep disturbance and quality problems, via pain in those areas.
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Mine too. I mean diagnosed medical specialist has looked at or diagnosed or suggested an investigation into almost each of those areas. I get pain in other areas (calf and shin was always the thing) but not to the injury sense, in a PEM sense.

Random sidenote, partly because I think this was mentioning in passing on the @James Cox thread about pain

I rely on heat a lot for pain. So have for many years now thank goodness had electric throws and heatpads (before that it was hot water bottles and when you need so many of those it isn't ideal for ME/CFS). Like it being common that most days over the years I might have several heatpads and a throw. Due to injuries etc and even in summer which was frankly horrific if it wasn't better than the summer before with x numbers of even worse in summer hot water bottles meaning I was 'could be worse'.

Recentlyish I for the first time in maybe nearly a decade had a window for more than days where I wasn't using a heatpad in my bed most days, just the throw. For various reasons. But I still use the throw because the bottom half of my legs get ice cold for one, in the last months it has been a joke of it being off and on as well because on the random hot days even the extra layer when it was off was too much,, but as it is only spring night was then cold.

Anyway here is the weird thing after what might seem like preamble but has context. I was getting hot flushes. I'd put the throw on 7 for 2 timer-wise (when I'd previous think nothing of level 9 for the higest time setting) and then even though the throw was mainly from hip down find I was burning up from that known area at the top of the chest just above the breast (isn;t that where the brown fat is and it is know to be a heat thrower area) up neck.

Now I get poor temperature regulation because I've had that for decades but this was different so I was starting to assume maybe it was a sign of my age as a woman and/or medication changes etc. as it had been a few months. And was starting to get cautious with the throw, even though it then happened of course if I put a jumper on because the hotter bit of my body was getting extra cover (where the heating the toes always worked better).

What I hadn't put it together with was that I was getting this at the exact same time I stopped using the heat pads that I often sit on and have on my legs, back etc maybe arms. I assumed adding these back in would be worse.

Until I had to sit somewhere else where, because everywhere in my home is set up as such, I switched on two heat pads in those areas on pretty hot. And I've now done that many times over. And I don't get any more overall hot by those than I did before.

I've now got my large heat pads back in my bed and put the electric throw on my feet on and I'm not getting the 'flush' or sudden burning up under the chin either. So it mainly seems to be a phenomenon that happens when the throw which goes over my quilt and my hip-to-feet is on and nothing else (which tend to be in direct contact, often on my rear side as it is back and legs etc). I mean I might get sweaty in situ but it isn't causing the under the chin flush. Plus I'm so much more comfortable - I forgot what a relief the direct heat round that area is.

You'd think a hotter thing nearer the top of your body would cause that same thing worse but it isn't and actually seems to make it less likely when the throw on the feet is on and warming those from on top (done in that area for warmth of icy toes rather than pain specifically, but it does ease eg calf and shins).

I thought nothing could surprise me anymore re: temp control because I had decades of it (but now those decades seem more logical than this even, at least I could eg trace back to things that made sense to me in a pattern) but there is 'another one'.
 
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My pain is often triggered by getting cold (and after going outside in my wheelchair I often struggle moving at all due to the cold) and sometimes fully disappears if I heat it up enough. Bath is amazing for leg pain but very exhousting.

Its odd. But I will say that I am unsure if I even have ME/CFS due to the number of other conditions I am uncovering this year!!
 
There was an issue that some data/screenshots from the presentations of the Berlin conference could not be made public yet. We have therefore deleted all our posts and our blog article about it. Apologies for the error.

Videos of the presentation will be made available later by the ME/CFS Research Foundation in a correct/vetted format. We will check and see if it's possible to share our summary of some of the talks afterwards.
 
Sorry if this has already been discussed, I don’t have the energy to read the entire thread.

But the impression I got is that after further analyses the DecodeME team seemed very confident in the original MAGMA analysis finding that the gene expression of the affected genes is by far most relevant in the brain.

I’m wondering now that we have “confirmation”, at what point can or should we start calling ME/CFS a neurological illness? At what point can I stop getting annoyed when advocates call it that hahah. I’m pretty sure neuroimmune is still a bit of a stretch given the current evidence. But neurological? Have we reached that threshold?
 
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