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Possible Brain Biomarker for ME/CFS Found

Antares in NYC

Senior Member
Messages
582
Location
USA
I remember, especially in my early years of ME/CFS, I had some intriguing language difficulty phenomena: in addition to forgetting words, losing vocabulary, and having sudden difficulty in spelling words, perhaps the oddest language symptom I experienced was the frequent selecting of incorrect words while talking, often in a bizarre way, where I would select a word which was incorrect, but the incorrect word was from the same category as the right word – for example, I might incorrectly say “pun” when I meant to say “irony” – both are in the same category of literary devices.

Has anyone else had this, where you say the wrong word, but that wrong word is from the same general category as the right word that you should of said?

ALL. THE. TIME!

To this day, it keeps happening to me since day one. Constantly and inadvertently replacing words of the same general category. Odd and very, very frustrating.

This has actually made me much more self-aware and introverted. Before CFS I was an avid public speaker. After CFS I'm terrified to speak in public because I know there will be a huge difference between what I wanted to say and what comes out of my mouth.
 

WillowJ

คภภเє ɠรค๓թєl
Messages
4,940
Location
WA, USA
Before I developed ME/CFS, I used to use the supplement acetyl-L-carnitine (ALC) to improve verbal fluency in writing. I read some research that found ALC was a smart drug (nootropic) which increased language and verbal abilities.

...

Nowadays, for my ME/CFS, I take 1000 mg of ALC daily, as an antioxidant. If I don't take ALC daily, I find I develop a craving for chocolate, which is a good antioxidant that has been shown beneficial for ME/CFS. So somehow I think ALC has the same antioxidant effect in my brain as chocolate, but without the calories.

I need the calories, so am I doing just as well to eat dark chocolate every day?
 

WillowJ

คภภเє ɠรค๓թєl
Messages
4,940
Location
WA, USA
There have been far more significant studies showing that this is a "real" condition. I suppose we're getting over-the-top headlines and media coverage because this is coming from a Stanford press release.

they might have spent money sending it over the newswires :D
 

taniaaust1

Senior Member
Messages
13,054
Location
Sth Australia
I'm the same and I also have problems talking full stop when I am at my worst. I know what I want to say but I can't. Interesting as I had thought it was all left side but clearly it's not actually clear cut - thanks to those who posted on that above.

This study could be important, but we won't know unless someone tries to replicate it in a larger group. Not knocking the study though, I'd rather have a small study than no study.

I'd have thought brain scans might be more reliable than things like cytokine markers which fluctuate and are prone to different methods affecting results. But I don't know much about these kinds of brain scans. Anyone with more knowledge on the consistency of such scans?

There is a current brain study being done in Adelaide, South Australia which Im in and I hope is nearing completion (im not sure when its due to be completed, its a follow up brain study on past brain study results to see if our brains with the ME/CFs are getting worst with time etc), it is looking at the mid brain and the white matter. In the first study they found that the longer one has had ME/CFS the more ones midbrain had shrunk.

Hopefully the researchers hear about this study and try to compare this study with their current scan results. (maybe I should phone (if I can find the phone number) the head researcher and make sure he knows about this one but right now Im feeling quite bogged down with things so probably wont try doing that).
 

Min

Guest
Messages
1,387
Location
UK
There is a current brain study being done in Adelaide, South Australia which Im in and I hope is nearing completion (im not sure when its due to be completed, its a follow up brain study on past brain study results to see if our brains with the ME/CFs are getting worst with time etc), it is looking at the mid brain and the white matter. In the first study they found that the longer one has had ME/CFS the more ones midbrain had shrunk.

Hopefully the researchers hear about this study and try to compare this study with their current scan results. (maybe I should phone (if I can find the phone number) the head researcher and make sure he knows about this one but right now Im feeling quite bogged down with things so probably wont try doing that).
Please do try to find the energy and time. Thsnk you
 

Simon

Senior Member
Messages
3,789
Location
Monmouth, UK
[re arterial spin labelling not finding any difference in perfusion]Are there many other studies that look at perfusion? I always thought this was important as a possible cause of cognitive difficulties and orthostatic intolerance. I assume the participants were laying down. What would they see if the participants were standing?
Good question. The blood flow experiments I'm most aware of are those by Medow/Stewart (eg Phenylephrine Alteration of Cerebral Blood Flow During Orthostasis; Effect on N-Back Performance in CFS)
looking at patients who also have orthostatic intolerance (which is probably a minority of patients). They find that reduced blood flow on tilt/standing is associated with poorer cognitive performance, so maybe the STanford study would have found similar if they'd measured perfusion on standing.

Most MRI is done with subjects lying down (because of the nature of these huge machines) and Medow/STewart didn't use MRI to measure blood flow.
 

Sidereal

Senior Member
Messages
4,856

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
from post 109
Overall white matter volume was significantly reduced globally ME/CFS patients brains with a trend towards a specific reduction in the thalamus. Because the white matter, or the wiring in the brain, is particularly susceptible to inflammation, inflammation – perhaps sparked by a viral infection – was likely causing the global white matter reductions found.
(my underlining)

This is a possible interpretation. There is another though. First a caveat: I have yet to read the full study, so my interpretation may change later.

White matter is about connections. One of the processes that goes on in the brain is an increase in connections between active areas. The other is the opposite - low activity areas lose connections.

While I think an inflammatory or other immunological process might be happening, just decreased brain activity alone might cause a decrease in white matter over time. There are two consequences here. First, its an indicator of long term brain fog - reduced brain activity. Second, its reversible, though not necessarily quickly reversible. If this is what is happening then as brain function is restored at least some of the white matter would be restored over time.
 

lansbergen

Senior Member
Messages
2,512
Second, its reversible, though not necessarily quickly reversible. If this is what is happening then as brain function is restored at least some of the white matter would be restored over time.

If one or more tested patients improve they should be tested again.
 

Research 1st

Severe ME, POTS & MCAS.
Messages
768
This study is great to see, especially as already commented on in relation to the previous Japanese 'ME' research and equally fascinating to me as it was previously found that BDNF(Brain-derived neurotrophic factor) was found to be abnormal in CFS patients (alongside MS) by American researchers.

Source (Sorenson et al, 2014):
http://omicsonline.org/neurology-neurophysiology-abstract.php?abstract_id=25722


Perhaps the participants in this study with these abnormal DTI brain scans at Stanford (Dr Montoya's team) could have their BDNF tested too? (Dr Leonard Jason was involved in the CFS vs MS BDNF paper linked above).

I say that as this brain imaging study found a possible marker for neurodegeneration, and BDNF is also a marker for neurodegeneration. I wonder if this is all PrPC related, as in absence of enough PrPC?


One hypothesis could be the ME CFS brain is lacking PcPC, and is atrophying due to accelerated oxidative injury to tissue. Some evidence for this exists in repeated studies, at least in the blood due to the high levels of oxidative stress found. Uncontrolled this is hazardous to ME CFS patients, as this can lead to endothelial damage, the endothelium being the lining of blood vessels. We don't want this as plaques can form (oxidised fat or calcium) leading to possible heart attacks or strokes.

Focussing back on PrPC for the patients reading this with severe ME who are interested in their own testing, I would consider contacting REDLABS in Belgium who offer an experimental PrPC test. They have a normal prion protein estimation assay for a very reasonable 75 Euro cost ($94) if you can get your sample there within 24hrs from your location:

Source: Experimental prion protein estimation (PrPC).
http://www.redlabs.be/red-labs/ordering-tests/request-forms.php


I tested mine and it was extremely low, and I've heard other patients with severe ME CFS also have very abnormal results. It would be good if REDLABS could develop such as prion protein test (misfolded proteins), e.g. PrP 'something'....and make this available to patients and the research community. Although it's interesting to see one has very low (some have high) PrPC what we really need is to then show, that a rogue prion is transcribing this normal PrPC into something more sinister. Then scientists can try and find why. Borrelia? HERV's? Retroviral Genes? etc etc.

Very low PrPC coupled with this latest brain scan technology and the BDNF reduction may well show that people diagnosed with ME CFS (and likely Chronic Lyme) actually may develop some form of neurodegeneration over many years, which could well explain progressive ''brain fog'' and/or other neurocognitive phenomena currently ignored by the wider medical profession, or by the radicals as ''functional'' disorders of the mind.

When science is permitted to go ahead into the complex nature of ME CFS, it's great to see the results. Ground breaking, quality ME CFS biomedical research may even feel like a motivational force for patient to focus on in terms of trying to keep up a positive mental health state. A recognition that some scientists (albeit in little underfunded groups) really are on the right track, or at least, potentially there.

I know I'm grateful for these scientists work and I'm sure others are too. We just need more of it, and to cancel the P2P and IOM contract ASAP and get down to the real hard facts.

Acquired neurological disease. That shouldn't be a taboo.
 
Last edited:

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
While I cannot rule out prions, misfolded proteins are not necessarily the same as a prion disease. Proteins misfold in excessively alkaline or acidic environments. They also misfold when glutathione is depleted. We have all these issues. Oxidative environments might also do it. Prions are, to current understanding, a rare cause of misfolding, but devastating when they occur and prion proteins accumulate.

Further if there is damage to cellular capacity to degrade improperly folded proteins this can lead to accumulation.
 

lansbergen

Senior Member
Messages
2,512
While I cannot rule out prions, misfolded proteins are not necessarily the same as a prion disease. Proteins misfold in excessively alkaline or acidic environments. They also misfold when glutathione is depleted. We have all these issues. Oxidative environments might also do it. Prions are, to current understanding, a rare cause of misfolding, but devastating when they occur and prion proteins accumulate.

Further if there is damage to cellular capacity to degrade improperly folded proteins this can lead to accumulation.

Prof Laura Manuelidis prion papers

www.ncbi.nlm.nih.gov/pubmed/?term=laura+manuelidis
 

osisposis

Senior Member
Messages
389
haven't read these but may give some insight, I've said all along this is TBI, like closed head TBI


Effects of Practice and Experience on the Arcuate Fasciculus: Comparing Singers, Instrumentalists, and Non-Musicians

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133864/

A Review of Magnetic Resonance Imaging and Diffusion Tensor Imaging Findings in Mild Traumatic Brain Injury


the “miserable minority,” the cognitive and physical symptoms do not resolve following the first three months post-injury. Instead, they persist, and in some cases lead to long-term disability. The explanation given for these chronic symptoms, i.e., postconcussive syndrome, particularly in cases where there is no discernible radiological evidence for brain injury, has led some to posit a psychogenic origin. Such attributions are made all the easier since both post-traumatic stress disorder (PTSD) and depression are frequently co-morbid with mTBI.


We would argue that the controversy between mTBI being psychogenic versus physiogenic in origin is not productive because the psychogenic view does not carefully consider the limitations of conventional neuroimaging techniques in detecting subtle brain injuries in mTBI, and the physiogenic view does not carefully consider the fact that PTSD and depression, and other co-morbid conditions, may be present in those suffering from mTBI. Further, patients with mTBI may complain more when their symptoms are not validated. That is, when there is no radiological evidence that explains their symptoms, and yet they still experience symptoms, these patients may complain more because of the lack of validation, versus those patients who have radiological evidence that validates their symptoms, leading them to complain less, simply because they have a medical explanation for their symptoms.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3803157/
 

osisposis

Senior Member
Messages
389
Effects of Practice and Experience on the Arcuate Fasciculus: Comparing Singers, Instrumentalists, and Non-Musicians


This might suggest that the right AF shows more of a domain general adaptation effect in activities that involve matching sounds with actions independent on whether these actions are articulatory actions or hand actions. The left AF and in particular the dorsal branch of the left AF showed the most profound differences comparing singers with instrumentalists. Although this finding is somewhat surprising, it suggests that the left AF, which already shows an adaptation when individuals acquire language (Barnea-Goraly et al., 2005; Ashtari et al., 2007) and is usually larger and more complex than the right AF (Vernooij et al., 2007; Glasser and Rilling, 2008), might be the structure that adapts the most to the specific requirements of vocal–motor and auditory–motor integration

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3133864/

A Review of Magnetic Resonance Imaging and Diffusion Tensor Imaging Findings in Mild Traumatic Brain Injury




http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3803157/