[ME/CFS Research Foundation] International ME/CFS Conference 2026 on 7–8 May - register for free now!
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Venicequeenf
Established Member (Voting Rights)
Did they say it about the IA (as it is not included in the inclusion criteria)?
jnmaciuch
Senior Member (Voting Rights)
Sorry if this is a redundant question, havent had time to follow closely. I vaguely remember from some lecture or presentation I attended a while ago that TSPO tracers have quite high binding affinity to some peripheral proteins. Idly wondering if this could be a possible explanation for reduced brain signal in James’ results. Would appreciate if someone could let me know whether the presentation mentioned anything about accounting for peripheral binding fraction somehow
ScoutB
Senior Member (Voting Rights)
I didn’t get a chance to watch yet either but @ME/CFS Science Blog did say this on bluesky:
“She says this has been observed before in schizophrenia and depression. She thinks this is due to peripheral inflammation inhibiting the TSPO tracer from going to the brain.”
Bsky thread
Bettina Grande now made the conference posters available:
Yes, that was mentioned in the German presentation.
This slide only lists autoantibodies as a prerequisite.
Let’s wait and see what the requirements are when the study begins!
It’s interesting to note that there were also sponsors from the pharmaceutical industry this year (at the very bottom of the page).
events.mecfs-research.org
ME/CFS Research Foundation
events.mecfs-research.org
jnmaciuch
Senior Member (Voting Rights)
Thank you!
Jonathan Edwards
Senior Member (Voting Rights)
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?
V.R.T.
Senior Member (Voting Rights)
I noticed that - hopefully it's a sign of real interest in the field.It’s interesting to note that there were also sponsors from the pharmaceutical industry this year (at the very bottom of the page).
ME/CFS Research Foundation
Felis Catus
Senior Member (Voting Rights)
Me, too. It's good to see someone as big as Bayer who also happens to have HQ and big R&D in Germany. Great things might happen if the national decade money goes to the right hands*. Enthusiasm is contagious!
*I mean to the researchers in academia. Bayer has enough money.
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Murph
Senior Member (Voting Rights)
This seems to be a newish finding confirmed in a paper published only two weeks before the conference. And their interpretation is not about more of the tracer being consumed in the periphery, moreso about BBB function.
https://pubmed.ncbi.nlm.nih.gov/42034206/
"...The study confirms that increased peripheral inflammation is associated with reduced blood-to-brain transport of TSPO tracers, suggesting a role for blood-brain barrier permeability in the observed effect."
Murph
Senior Member (Voting Rights)
I quite like this idea.
The good thing about a pathogen persistence theory is you probably don't need to worry so much about the WASF3, the eif2alpha, the interferons, the Th17s, and the PANX-1, etc. If a pathogen persists you've probably found a good upstream explanation for all those bits of the elephant researchers are currently groping for.
And a target to pursue.
I wonder if any incidental CAR-T therapy mecfs remissions/recoveries exist. Some of the trials I'm seeing online are in very sick people where it's like, in our n=8 trial, 4 patients died and our study shows wonderful safety and efficacy. Hinting that they're not handing out car-t cells to just anyone yet.
edit: But there's also this:
CD19 CAR-T cells for treatment-refractory autoimmune diseases: the phase 1/2 CASTLE basket trial
They apparently put people from three different diseases in the "basket" and almost all of them went into remission."22 of the 24 patients achieved predefined efficacy endpoints, with 9 out of 10 patients with SLE reaching DORIS remission, 9 out of 9 patients with SSc showing no disease progression, and 4 out of 5 patients with IIM reaching ACR major/moderate response."
I'd be interested to be a basket case myself.
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Not that we know of. This therapy is much cheaper in China, so I imagine it won’t be long until we have a volunteer and a willing Chinese CAR-T practitioner.
DMissa
Senior Member (Voting Rights)
Yes, we are both interested in this stuff, we recently discussed it a bit and where I have small bits of spare time I am working on developing project outlines. Broadly, yes any lipid class that has a role in cell membrane composition could tie into some of the ideas and suspicions some of us have.
I am only vagueposting because a) I don't want people to get carried away with untested specifics and b) I am still learning about those specifics
DMissa
Senior Member (Voting Rights)
The problem is that "metabolism" is very broad. What exactly are we referring to here?
I do not think a primary, systemic failure of respiration is likely.
I do think that studies profiling the levels or usage of lipids in different immune populations have shown more consistent differences than tends to occur in this field. This may be a simple reflection of other alterations in these cells but it could be the reverse as well. Altered membrane composition can change BCR and TCR affinities. Accumulation of certain species in membrane can elicit immune responses. There is a substantial field of fundamental biology behind this and there are too many possibilities to list.
Whether it ends up being important or not, there is some signal appearing in the literature that can either cause or arise from events that may be relevant to a disease process. That is at the very least worth following up in specific terms to dissect cause from effect and to validate whether anything is changed in reliable, targeted assays of primary patient samples
Of course there are all of the other ideas around nitrogen metabolism or glycolysis based mostly on biofluid data (If I remember correctly) but I only comment here on what I have the greatest knowledge of
Jonathan Edwards
Senior Member (Voting Rights)
Agreed, everything is metabolism in a way. And I agree that lipid shifts in specific cells may be very interesting. It is more general pathways that I think have been studied enough to think are probably working normally.
leokitten
Senior Member (Voting Rights)
The industry is trying to find new approaches for "off the shelf" CAR-T that produce as good efficacy as autologous. So far the allogeneic approach has not worked as well, so now a lot of companies are pushing hard into new in-vivo CAR-T approaches.
In-vivo CAR-T promises a cheaper and faster process as well as no lymphodepletion. This would dramatically lower the costs and risks associated with trialing it in new illnesses. I hope this technology works out
www.nature.com
In-vivo CAR-T promises a cheaper and faster process as well as no lymphodepletion. This would dramatically lower the costs and risks associated with trialing it in new illnesses. I hope this technology works out
In vivo site-specific engineering to reprogram T cells - Nature
Stable and cell-specific transgene expression can be achieved through in vivo site-specific integration of large DNA payloads using a two-vector system of enveloped delivery vehicles and adeno-associated viruses.
www.nature.com
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ryanc97
Senior Member (Voting Rights)
I’m quite sure it’s like tens of thousands of dollars, more than Dara for sure. Like 50k? Idk