Webinar - ME/CFS Involves Brain Inflammation: Results from a Ramsay Pilot Study - Jarred Younger

Wasn't able to view it today - if this is available after, if anyone would be kind enough to share the link I'd love to view it still.

Likewise if anyone has any takeaways I'd love to hear them.

 

I left the webinar with the impression that higher quality research into ME/CFS is being conducted compared to 5 years ago.

 

I have not looked at the webinar but am trying to catch up with the earlier discussion.

One point worries me. Inflammation is associated with a rise in temperature of the organ involved if that organ is normally at below core temperature. In other words hands and feet get hot with inflammation but I am not at all sure that a liver or a brain would get hot. The 'heat' of inflammation is due to more blood at core temperature flooding in to tissues that are normally colder. If a tissue is normally at core temperature - as brain is - then the increased blood flow of inflammation would not be expected to raise the temperature. It might even help cool the tissue down a bit.

Temperature might also rise because of cellular activity but brain cells are about the most metabolically active in the body anyway. I suspect microglia have very low energy requirements in comparison.

In other words, although it would be fascinating if brain was at a different temperature in ME I rather doubt it would indicate inflammation.

 

Moderator note: Post moved from another thread

Just watched the SMCI webinar with Dr. Jarred Younger, presenting the results of his Ramsay fund (from SMCI) study on neuroinflammation. Thus far, his hypothesis that ME involves brain inflammation has been verified.

The study has been through peer review, and will be published in about a month or so in the journal Brain Imaging and Behaviour.

This is of course a small study to start with: 15 with ME; 15 controls. Significant signs of neuroinflammation in pwME, and not in controls. The specific stats will be released by the journal.

Jarred is applying for more funding, collaborating with researchers new to this field, keeping track of neuroinflammation research in other fields, such as Alzheimer's, Autism, and epilepsy.

He said three other previous studies have found neuroinflammation in pwME, however, their ability to research chemicals that cause the inflammation was more limited.

He is also looking at herbs reported to reduce inflammation. This is double blind, and still in process.

The brain imaging he is using is an MRI with an extension to examine chemicals that cause inflammation. Two of these found to be significant in this study are lactate and choline.

As regards an ad for ME; another wild and crazy idea: there was an ad about "your brain on drugs", that showed fried eggs in a frying pan. How about a photo of a brain scan showing neuroinflammation in ME: "your brain with ME", the "ME brain", the "ME brain on fire"...

Jarred Younger is an excellent presenter. SMCI said the number of registrants for this webinar far exceeded any previous ones.

 

A couple more points about Jarred's webinar: he said clinician/researchers are already coming to him with requests on how to do this more complex MRI testing.

He hopes that with more data, this technique will be able to distinguish between various brain injuries/diseases. He showed an image of a concussed brain which looks different than ME brains.

His study did not find elevated levels of N-acetylaspartate which I understand can cause brain damage like that seen in MS.

 

That is what is puzzling, because by definition inflammation is associated with increased blood flow, so that should cool the brain down, rather then heating it up.

I am pretty sure the metabolism of microglia will be quite slow in comparison to neurons, which use huge amounts of energy for electrical signalling. So an increase in local brain temperature would be better explained by an increase in nerve cell activity rather than inflammation.

 

Jarred is an excellent speaker.

I think people could relate to the brain images, and see this as important, and why ME has multiple symptoms, which is why I think ads about this area of research and findings could be effective, and why I included my summary of the webinar in this thread. I've missed stuff too, so thank you for your notes!

More research of course needs to be done - larger subject numbers etc., but pointing out the link to the new study, with photos would, I think be somewhat effective, if not for the public, then for those in medicine.

 

Does the increased nerve cell activity cause the excitotoxicity Cheney talks about....my symptoms calm with Klonopin and I can be more functional for a short time...it's like the old me comes back. Also, I wonder if increased nerve cell activity causes the wired feeling at night, the racing brain? Im not convinced by Jarred Youngers hypothesis, I think there's more going on, that's my tuppence worth as a patient. Plus he is looking at mild to moderate patients, not the severe. So maybe alot more going wrong in severe spectrum

 

I think Jarred's research is exciting. Judging from the large attendance for this webinar, others are quite interested as well.

 

Solve do seem to post their webinars on YouTube so I'll look forward to seeing this one - it sounds very interesting.

 

For those pwme whos heads are burning with anticipation, an early copy of the webinar can be found here:

 

Disclaimer: I had to skim through the video so I could have misunderstood.

In the video, Younger specifically talks about the heat mapping with areas of increased lactate and choline. He seems to have identified increased chemicals in the brain first, and then correlated this with the hot spots so that the MRS can be used non-invasively to measure chemical increases.

When he mentions neuroinflammation, I don't think he uses it in the same way other people use the term 'inflammation'. I.e., while inflammation seems to increase blood flow to an area, this appears to be the opposite.

What he means is overactive cells (microglia, mostly) producing too much choline or lactate because of a speeded up process of cell replacement, and increased aerobic metabolism in the brain (respectively).

He thinks that cells are dying too quickly, and therefore being replaced too quickly, which increases the choline, while aerobic metabolic processes are also speeded up, so that an excess of lactate is accumulating.

It's this 'brain on fire' idea again. Notably, he doesn't think there's neuronal death.

 

Yes, this is as I understand it and seems to be confirmed by your quotes.

 

I think that is indeed what he thinks but I think it would help the scientific process in general to say that rather than talk of 'neuroinflammation'. The query I have is why increased cell activity and lactate production should be attributed to microglia rather than neurons, which have a much higher metabolic rate normally. And I am not clear what cells dying and being replaced would have to do with it.

I didn't think aerobic processes generated lactate. I thought they generated CO2 and water through the Krebs cycle.

 

This is all way over my head and I still haven't watched the video but

so it would be great to make progress on getting to the bottom of the mechanism, with questions like these:

Can we contact Jarred Younger? Can we invite him to a post-publication discussion of his work here on S4ME? (Not sure if we still have the capacity for that, @Andy?)

It bothers me that researchers may be silo'ed off from each other in such a way that a full discussion of their findings from all angles doesn't always seem to happen at an early enough stage. If this brain-heating is a genuinely exciting observation (and it seems like one to my inexpert eyes) then it would be great to get it thrashed out in a big discussion.

 

Funnily enough, it's already on my to-do list.