Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation (2018) Albrecht et al.

Interesting. It looks a well planned study at first glance. The data are plausible and would be very significant if confirmed.

 

One of the two studies was done in the workplace of van Elzakker who is currently conducting a ME/CFS study with the same radioligand. So the methods should be similar and maybe even improved.

 

Nice to see a range of converging evidence all pointing to the microglia.

 

I found the following passage interesting with respect to a potential two (or multi)- hit model of onset (MIA = maternal immune activation) :

httpsw.nature.com/articles/tp201780://ww

While this relates to a mouse model of schizophrenia (and subsequent treatment with minocycline) , pre-natal priming of microglia could set up a situation where a later environmental insult (e.g. physical in fibromyalgia or viral in ME/CFS) appears to be the initial trigger rather than one of many possible triggers that tip already primed microglia into a chronic activated state?

 

Merged thread

Source: EurekAlert

Date: September 27, 2018

URL:
https://www.eurekalert.org/pub_releases/2018-09/mgh-rtf092718.php

Research teams find widespread inflammation in the brains of fibromyalgia patients
----------------------------------------------------------
PET imaging studies at Mass. General Hospital, Karolinska Institutet reveal elevated glial activation, correlation with fatigue levels

A study by Massachusetts General Hospital (MGH) researchers - collaborating with a team at the Karolinska Institutet in Sweden - has documented for the first time widespread inflammation in the brains of patients with the poorly understood condition called fibromyalgia. Their report has been published online in the journal Brain, Behavior and Immunity.

'We don't have good treatment options for fibromyalgia, so identifying a potential treatment target could lead to the development of innovative, more effective therapies,' says Marco Loggia, PhD, of the MGH-based Martinos Center for Biomedical Imaging, co-senior author of the report.

'And finding objective neurochemical changes in the brains of patients with fibromyalgia should help reduce the persistent stigma that many patients face, often being told their symptoms are imaginary and there's nothing really wrong with them.'

Characterized by symptoms including chronic widespread pain, sleep problems, fatigue, and problems with thinking and memory, fibromyalgia affects around 4 million adults in the U.S., according to the Centers for Disease Control and Prevention. Previous research from the Karolinska group led by Eva Kosek, MD, PhD, co-senior author of the current study, suggested a potential role for neuroinflammation in the condition - including elevated levels of inflammatory proteins in the cerebrospinal fluid - but no previous study has directly visualized neuroinflammation in fibromyalgia patients.

A 2015 study by Loggia's team used combined MR/PET scanning to document neuroinflammation - specifically activation of glial cells - in the brains of patients with chronic back pain. Hypothesizing that similar glial activation might be found in fibromyalgia patients as well, his team used the same PET radiopharmaceutical, which binds to the translocator protein (TSPO) that is overexpressed by activated glial cells, in their study enrolling 20 fibromyalgia patients and 14 control volunteers.

More at
https://www.eurekalert.org/pub_releases/2018-09/mgh-rtf092718.php

 

@Simon M @JaimeS @Andy @adambeyoncelowe @Inara
@Perrier


August 24, 2018 : One more target (TSPO Gene) identified previously by Machine Learning :






So far, Machine Learning was able to identify before any other Researcher these potential targets :

-Pyruvate Dehydrogenase (Fluge et. al)
-Phospholipid Metabolism dysregulation (Hanson et. al, Naviaux et. al)
- Fas Ligand (FASLG - Michael Sakora)
-Possibly impaired Liver function (Hanson et. al)


@Graham i would like to argue that there is a "Matrix" involved in ME/CFS Research as you suggested. It's the Selfish Gene at play.

 

Merged thread

https://www.sciencedirect.com/science/article/pii/S0889159118302423?via=ihub#b0175

Very interesting article about neuroinflamation in FM, using PET-MRI with a tracer for glial activation.
I think it has lots of interesting information regarding LDN, Duloxetine and how to asses brain inflamation.
It also refers to the work of Jared Younger and Dr Nakatomi, from Japan.
There is Glial activity dected in the Cingulated Cortex in this FM study and in the Nakatomi study; and in this sudy this activity is associated with the severity of fatigue.

 

Brain Inflammation Imaged for the First Time in Fibromyalgia

https://www.dailykos.com/stories/20...ion-Imaged-for-the-First-Time-in-Fibromyalgia

 

May I ask those who’ve been following FM research, is the evidence base for neuroinflammation in FM and stronger than in ME?

 

I would argue against using the term neuroinflammation. It is a buzz word with too little precision. The 2018 study suggested some microglial activation. That does not amount to inflammation. I am not ware of anything much being reported since but I don't search on fibromyalgia.

 

Ok, just wondering in relation to the recent Younger DXM trial not showing significant efficacy and whether the FM evidence base on microglial activation was stronger than in ME. They chose DXM because it inhibits microglia so wondered if it was a surprise that it didn’t work.

I personally have trialed multiple drugs that supposedly inhibit microglial activation and, like most others with ME, got no benefit from them. Even if we see microglial activation I think the research community doesn’t yet know what to make of it.

 

The other thing as @Jonathan Edwards the (Japenese) study, which found evidence of microglia activation, hasn't been replicated. Also, they used an old (not very specific) binding agent in that study; it was supposed to be replicated with one of the newer (more specific) binding agents but I don't recall a published second study.

 

Hopefully this study will get published soon. They did a talk at a conference last year. I believe it does replicate some of what Nakatomi et al. found and I believe they used a 2nd gen radiotracer [11C]DPA-713 (Nakatomi used a 1st gen)

https://www.s4me.info/threads/tspo-pet-mri-reveals-increased-neuroinflammation-in-basal-ganglia-in-chronic-fatigue-syndrome-patients.16206/