Decadelong low basal ganglia NAA/tCr from elevated tCr supports ATP depletion from [Mt] dysfunction and neuroinflammation in [GWI], 2025, Cheshkov+

[Utsikt]

Fluge and Mella, the principal investigators of the DARATUMUMAB trial, explicitly discuss autoantibodies against beta-receptors as a potential pathomechanism in ME/CFS. You can read it here:

Potential being the key word here. In reality, we have no clue.

Yes, the Mitodicure drug is largely based on hypotheses. However, Wirth did show that serum from ME/CFS patients induced muscle weakness in rats, and the experimental drug was able to reverse that effect. So at least in rats, there seems to be a measurable effect.

Lots of things can induce lots of effects in rats, and it rarely translates to humans. Did they use serum from both healthy and diseased controls to show that this effect is unique to ME/CFS serum?

Another possible mechanism is molecular mimicry. Scheibenbogen published a paper on this. Autoantibodies can persist even after the virus is gone, because the immune system has been “trained” to react to the body’s own proteins.

You might want to take a look at this response by Jonathan Edwards about the fundamental issues with molecular mimicry theories.

Preprint Post in thread 'Molecular Mimicry Between Epstein-Barr Virus and Human Herpesvirus-6 Proteins and Central Nervous System Proteins..., 2025, Almulla, Maes et al'

Apr 14, 2025

What does mimicry actually mean? Does it mean that they different parts can interact with each other? And does that even matter?

The basic idea is that if a microbial protein is sufficiently similar to a host protein then the immune system can make the mistake of mounting a response to the microbial protein that also reacts with self protein. So if the microbial protein has a peptide sequence with letters for amino acids:

AQTGES

and there is a host protein with a peptide

AQGGES

then maybe T cells reacting to AQTGES will help B cells make antibody to AQGGES.

The only problem is...

• Jonathan Edwards

• 

I can see that I’m probably not going to convince you any further

I’m asking questions because you seem rather convinced about this hypothesis, so if I can understand the evidence you’re basing your assessment on, I might get a better understanding of why you are convinced or hopeful.

 

[poetinsf]

Link to research: Decadelong low basal ganglia NAA/tCr from elevated tCr supports ATP depletion from mitochondrial dysfunction and neuroinflammation in Gulf War illness

This sounds superficially similar to the recent talk in IACFSME conference about mitochondrial dysfunction causing ATP shortage in LC vesicles in brainstem, which in turn resulting in norepinephrine deficit and brain dysfunction:

Role Reversal: Could a WEAKENED Fight/Flight Response Be Causing ME/CFS and Long COVID? The 2025 IACFS/ME Conference Pt. I

by Cort Johnson
| Nov 11, 2025 |

Astrocytes, Autonomic Nervous System, Brain, Brainstem, Dopamine, Energy Production, Homepage, Locus coeruleus, long COVID, Neuroinflammation, Neuroinflammation, Norepinephrine, Oxidative Stress, Research, Sleep |

https://www.healthrising.org/blog/2025/11/11/fight-flight-system-chronic-fatigue-long-covid/