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

[Jaybee00]

Couldn’t find the abstract.

 

[wigglethemouse]

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.

 

[wigglethemouse]

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

I am in touch with Jarred - he’s wonderful! He’s currently imaging mild ME/CFS patients and I am imaging those with more extreme symptoms. We plan to share data and discuss and help each other with this important research

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

 

[Jaybee00]

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

 

[wigglethemouse]

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

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

All conference materials will only be available to registrants, unfortunately. But we are continuing this work, and will do our best to publish a paper when everything has been collected and analyzed!

 

[DigitalDrifter]

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

 

[Mithriel]

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.

 

[Jaybee00]

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.

 

[spinoza577]

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

Beyond its potential role as a transporter, TSPO could also act as a receptor or sensor, in line with its function in Rhodobacter where RsTSPO is part of a regulatory process that facilitates the switch between photosynthesis and respiration in response to changes in light and oxygen conditions. The role of RsTSPO in this signaling path appears to involve porphyrin transport and regulation of photosynthetic genes [21,22]; however, given the location of TSPO in the outer membrane of mitochondria in higher organisms, it is hard to visualize a similar stress response mechanism. In plants and cyanobacteria, it has been shown that the knockout of a TSPO homolog is significantly less sensitive to salt stress [56]. In contrast, when Arabidopsis is challenged with oxidative stress by porphyrin-induced cytotoxicity, TSPO overexpression protects against chlorosis [32, 57]. The role of TSPO in these stress responses remains to be determined. The elevated expression level of TSPO under various stressful conditions, such as oxidative stress, salt stress and inflammation in bacteria, plants and animals, suggests an evolutionarily conserved stress sensing or stress combating role for TSPO. Considering the ability of TSPO to bind and potentially transport porphyrin compounds, high levels of TSPO could provide a mechanism for alleviating oxidative stress, through favoring the removal [21,58] or degradation of porphyrin [27].

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.

 

[Simon M]

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.

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.

Region-of-interest analysis revealed that 11C- (R)-PK11195 [radiotracer] BPND values in CFS/ME patients were significantly higher than those in healthy controls in the cingulate, hippocampus, thalamus, midbrain, and pons and tended to be higher in the amygdala (Table 2).

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.