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Evidence of widespread metabolite abnormalities in me/cfs-whole-brain magnetic resonance spectrosco

Messages
52
Please don't despair. I haven't read the published paper yet, but in Dr. Younger's presentation, he said he was working to find a drug to treat this and thought Naltrexone might be close.

I'm very impressed with Dr. Younger. Not only is he doing great research, but like Dr. Davis, he is sharing it before it is published. Finally, he is looking for clinical solutions.
 

ljimbo423

Senior Member
Messages
4,705
Location
United States, New Hampshire
At the end of this video (it's only 21 minutes long), from last Septembers OMF symposium. At 18:35, Jarred Younger says that he just got a grant from the ME Research UK group.

To see if T cells and B cells are crossing the Blood Brain Barrier (BBB) and causing the brain inflammation in ME/CFS.

He said he should have the results hopefully, within a year. That would be by this September.

He says "if we can find these cells in the brain, it's going to be really, really important to understanding the pathology of ME/CFS."

 
Last edited:

Murph

:)
Messages
1,799
Great work here by Jared Younger and his team. He is rapidly ascending the ranks and he might be at this moment the researcher with the best flow of findings.

If I could summarise this paper I'd say they went looking for chemicals in the brain that might be evidence of neuroinflammation. They found plenty. They were able to specify the locations of various of these chemicals in different brain regions.

Looks like Choline was the most prominent, in the left anterior cingulate region.

Screen Shot 2019-01-11 at 10.09.47 AM.png


The most significant difference in the study was CHO in the left ACC. We note this area in particular because it is the only region to survive corrections for multiple comparisons, and because it has been noted as a critically important region mediating cytokine-induced fatigue and mood deterioration (Capuron et al. 2005; Harrison et al. 2009). Cytokineinduced fatigue and depressive symptoms have previously been attributed to inflammation in the ACC, as indicated by elevated glutamate on MRS (Haroon et al. 2014). The current study provides further evidence for the link between ACC inflammation and fatigue by demonstrating that ME/CFS patients show elevated CHO in this region.

The wikipedia on this part of the brain mentions autonomic functions which got me excited but mostly focuses on error detection and morality. It's hard to say if those are just things psychologists like to test or if those are really the core functions of this part of the brain. I don't feel we are especially morally deficient! Probably neuroscience is not yet really advanced enough to find regions of the brain that have very specific functions.

It's worth mentioning that in this study the observations are "normalised" by comparing to creatine levels. This looks to be standard practice but I can see an argument that creatine - an amino acid - could vary in patients. I hope Younger has a plan to rule out that as a potential source of bias.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
Here is a summary of this paper, by the UK ME Association:
https://meassociation.org.uk/2019/0...brain-inflammation-in-me-cfs-15-january-2019/

And here is another summary, by Solve ME:
https://solvecfs.org/research-and-r...h-grants/meet-the-researchers/jarred-younger/


this video (it's only 21 minutes long), from last Septembers OMF symposium.


And here is a transcript of the video:
https://www.omf.ngo/wp-content/uplo...unger-How-Brain-Inflammation-Causes-MECFS.pdf
 

Wishful

Senior Member
Messages
5,684
Location
Alberta
We keep having stuff pointed out about what’s wrong with us but no treatments to help any of it, this is starting to get me down

It's a complex problem, so any progress is valuable. If they can show that it's definitely a brain issue, they can stop wasting money on studies on blood, serum, muscles, etc. Likewise, the search for treatments can focus on the brain, rather than muscle mictochondria or antivirals or whatever else. Maybe if it can't pass the BBB, it's not a good candidate for ME.
 

Rufous McKinney

Senior Member
Messages
13,249
And here is a transcript of the video:

its felt, to me, that the brain is inflamed...for at least thirty years now. Including when I watched teh 2020 episode and they opened up the hole in the base of teh skull: where lots of my misery resides.

the idea the brain isn't inflamed or isn't capable of being inflamed makes no sense to me and never has.

That our brain is swollen makes total sense to me, and that what overheated and swollen condition is triggering numerous wrong messages being delivered through out the body..

that can be summarized as: My finger won't bend...
 

Nord Wolf

The Northman
Messages
564
Location
New England
Excellent research and I'll be very interested to follow its expansion and progress.
I had a high definition brain mri a week ago. I won't have the results presented to me until July 20th. I'm eager to see what they show, if anything. When I speak with the neurologist on the 20th I want to run this research by them, and the possibility of scheduling an MRS.
 

CSMLSM

Senior Member
Messages
973
Related discussions:

Dr. Jarred Younger shares his thoughts on how Covid-19 can cause psychological problems
https://forums.phoenixrising.me/thr...id-19-can-cause-psychological-problems.80885/

Jarred Younger Presents: How We Can See ME/CFS Inflammation In the Brain
https://forums.phoenixrising.me/thr...n-see-me-cfs-inflammation-in-the-brain.88061/
I would like to add from my own anecdotal experience that treating ME/CFS with an effective treatment does cause psychological problems. I believe from first hand experience that immune rebalancing occurs and underlying issues (infections) start to be addressed and obviously the brain is a major factor in this with microglia involvement and possibly EBV being the root cause of all this in some. I feel my ME/CFS is caused initially by EBV and some yet unknown genetic susceptibility like a receptor polymorphism or two in any number of systems.

The video of Dr Jarred Younger talking about psychological problems I have seen and I feel the immune response that should happen can cause this in the brain. So I am saying that treating this condition comes with the risk of psychological problems manifesting while that battle is going on and it happened to me many many times trying to fix this condition over the decades. I have succeeded now.

EBV has been detected in microglia.

Epstein-Barr virus is present in the brain of most cases of multiple sclerosis and may engage more than just B cells - PMC (nih.gov)
Abstract
Multiple sclerosis (MS) is a chronic neuroinflammatory condition of the central nervous system (CNS). It is a major cause of neurological disability in young adults, particularly women. What triggers the destruction of myelin sheaths covering nerve fibres is unknown. Both genetic and infectious agents have been implicated. Of the infectious agents, Epstein-Barr virus (EBV), a common herpesvirus, has the strongest epidemiological and serological evidence. However, the presence of EBV in the CNS and demonstration of the underlying mechanism(s) linking EBV to the pathogenesis of MS remain to be elucidated. We aimed at understanding the contribution of EBV infection in the pathology of MS. We examined 1055 specimens (440 DNA samples and 615 brain tissues) from 101 MS and 21 non-MS cases for the presence of EBV using PCR and EBER-in situ hybridization (EBER-ISH). EBV was detected by PCR and/or EBER-ISH in 91/101 (90%) of MS cases compared to only 5/21 (24%) of non-MS cases with other neuropathologies. None of the samples were PCR positive for other common herpesviruses (HSV-1, CMV, HHV-6). By quantitative PCR, EBV viral load in MS brain was mainly low to moderate in most cases. However, in 18/101 (18%) of MS cases, widespread but scattered presence of EBV infected cells was noted in the affected tissues by EBER-ISH. Immunohistochemical analysis of EBV gene expression in the 18 heavily infected cases, revealed that the EBV latent protein EBNA1, and to a lesser extent the early lytic protein BZLF1 were expressed. Furthermore, using double-staining we show for the first time that astrocytes and microglia, in addition to B-cells can also be infected. To the best of our knowledge, this is the most comprehensive study demonstrating that EBV is present and transcriptionally active in the brain of most cases of MS and supports a role for the virus in MS pathogenesis. Further studies are required to address the mechanism of EBV involvement in MS pathology.

I only hope to help others with my experience.