TSPO-PET/MRI Reveals Increased Neuroinflammation in Basal Ganglia in Chronic Fatigue Syndrome Patients

https://twitter.com/user/status/1290691765867966465


Couldn’t find the abstract.

 

It's a virtual conference taking place 8-14 August. You need to have credentials to log in for it.

 

It seems they are reporting on the Stanford study described in this thread that was trying to recruit mostly bedbound patients.
https://www.s4me.info/threads/stanford-neuroinflammation-study.6052/

In this April 2020 tweet from Michelle James Lab she describes that she is collaborating with Jarred Younger

https://twitter.com/user/status/1250231989522681857


This is a link to their Stanford University Lab web page and there is a profile on Mackenzie who is listed as a graduate student
http://med.stanford.edu/jameslab/team.html

 

Maybe now there are potential targets for pharmaceuticals?

e.g.

Neuroinflammation as a Factor of Neurodegenerative Disease: Thalidomide Analogs as Treatments

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6904283/#__ffn_sectitle

 

It has been confirmed that only registered participants will be able to see the presentations.

https://twitter.com/user/status/1291178291055951872

 

Does any one know what criteria they are using and what they class as "extreme symptoms"?

 

Problems in the basal ganglia have been found going back over twenty years. Good that this is being looked at again. One of these days some of this work will stick instead of just melting away.

 

https://forums.phoenixrising.me/thr...roinflammation-in-me-subcortical-brain.80923/

The first post here has a good explanation of the significance of this finding.

 

From Li et al 2015 PMC4567528/ doi: 10.1016/j.phrs.2015.03.022

Perspective: Evolving understanding of translocator protein 18 kD (TSPO)

page six says

I think this is very hot. It´s possibly a switch on and off for different energy productions, which could be crucial in the basal ganglia, say for encoding a forward firing vs a lateral firing or whatever. And it possibly reacts to salt stress, which would be in line with the Davis finding in white blood cells.

I think a malfunction of the basal ganglia could understandably account for a lot of symptoms, including downstream effects, or concomittant effects.

 

Yes, this is the same basic TSPO-PET MRI method as the Nakatomi neuroinflammation study indicating activation of microglia (see my blog). Though it's not clear if they use the same radiotracer to light up the glial cells (radiotracers have since got better, apparently).

However, the recent reports indicate new study lights up the basal ganglia, while the original Nakatomi study found other areas were lit up; nearby and interconnected areas, but so are a lot of things in the brain.

So it's interesting, but doesn't count as a replication, as far as I can see. Though I can't wait to see the paper. Both the Hanson group and Michael VanElzakker are doing/planning similar PET studies.