• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Long COVID patients have increased presence of amyloid deposits in skeletal muscle tissue, which was higher in long COVID and healthy controls after i

SWAlexander

Senior Member
Messages
1,962
Temporary findings: https://twitter.com/resiapretorius/status/1696272269641764949
Wonderful to see the @RobWust team at the #KSLongCoVID24 symposium. They found amyloid deposits, identified by ThT in the muscle. Perhaps due to movement of the amyloid deposits via the damaged vasculature?

Image
Image
 
Last edited:

Dude

Senior Member
Messages
193
This is what Herbert Renz Polster posted:
may be secondary to restricted perfusion, i.e. limited energy and oxygen supply - would be easy to test in an animal model looking at how healthy muscles (and other tissues) react to chronic redox imbalance. The tissue most sensitive to restricted perfusion may be neurons & glia.
It's kind of bitter that whatever you find, you first have to investigate whether it's not a cause of another event. Why does this disease have to be so complicated 😄
 

Osaca

Senior Member
Messages
344
This is what Herbert Renz Polster posted:

It's kind of bitter that whatever you find, you first have to investigate whether it's not a cause of another event. Why does this disease have to be so complicated 😄
Restricted perfusion is essentially what the whole "microclot theory" is about, so I don't really see what Herbert Renz-Polsters means when he's saying this, he's basically just reiterating what the dutch group is saying. Their whole work is based somewhere on those lines. From what I've understood the Amsterdam group has basically sold their work as "something wrong with oxygen supply, something wrong with mitochondria, we don't know more yet". Let's just hope deconditioning can be factored out completely.

Let's see what their dutch colleagues den Dunnen's animal model for Long-Covid will entail once it's published next month, although he seems to be focused on some newly discovered autoantibodies.
 

Dude

Senior Member
Messages
193
They plan to do similar research by the same team with MEcfs patients.
I see that PEM was a criteria for the LC subjects.
Is there any diffrence between Covid long hauler with PEM that fulfill the canadian criteria and OG Mecfs?
 

Osaca

Senior Member
Messages
344
They plan to do similar research by the same team with MEcfs patients.
I see that PEM was a criteria for the LC subjects.
Is there any diffrence between Covid long hauler with PEM that fulfill the canadian criteria and OG Mecfs?
Yes, the ME/CFS study is starting in the next few weeks, but till results are published it'll probably take a lot longer than a year.

One difference in their studies would be illness duration. Their ME/CFS study will first only be looking at pre-Covid ME/CFS, later on Long-Covid is included. That means their Long-Covid study where participants had an illness duration of maximum 1.5 years differs in duration from the ME/CFS study where the minimum illness duration is 3.5 years. That can have an impact on trivial things such as deconditioning or other things which their research could be pointing at, for example capillary rarefaction or mitochondrial changes. A big focus of their work are muscle adaptations which may change over time. We'll just have to wait and see.

They are also and have been for the pasts 3 years been applying for grants to study Long-Covid without success. Until now all their work has been funded by patient donations. I hope that these findings together with the IDO2 paper will be motivational enough for ZonMw for a proper grant, but the Netherlands hasn't shown any initiative to fund biomedical research for Long-Covid.
 
Last edited:

Osaca

Senior Member
Messages
344
As a patient who gets worse and worse, and never better then the day before.
Isnt deconditioning evident In symptoms ?
From what I can tell deconditioning wouldn't play a big role in their Long-Covid study. However, when looking at muscular markers, you have to try to ensure that what you are measuring isn't just some sign of inactivity or somehow correlates with it and as such inactive controls are always very appreciated.
 

SWAlexander

Senior Member
Messages
1,962
"They found amyloid deposits," What does this really mean?
No details yet on what kind of amyloid they found.

Amyloidosis is characterized by the accumulation of abnormal proteins known as amyloid fibrils in various tissues and organs throughout the body. Some common types of amyloidosis and the associated abnormal proteins include:
  1. AL Amyloidosis (Immunoglobulin Light Chain Amyloidosis):
    • Abnormal Protein: Immunoglobulin light chains (part of antibodies).
    • Source: Produced by abnormal plasma cells in the bone marrow.
  2. ATTR Amyloidosis (Transthyretin Amyloidosis):
    • Abnormal Protein: Transthyretin (TTR) protein.
    • Source: May be inherited with mutations in the TTR gene (hereditary ATTR amyloidosis) or occur sporadically with misfolding of TTR protein (wild-type ATTR amyloidosis).
  3. AA Amyloidosis (Amyloid A Protein Amyloidosis):
    • Abnormal Protein: Serum amyloid A (SAA) protein.
    • Source: Produced in response to chronic inflammation or infection.
  4. ApoA1 and ApoA2 Amyloidosis (Apolipoprotein A1 and A2 Amyloidosis):
    • Abnormal Protein: Apolipoprotein A1 (ApoA1) and Apolipoprotein A2 (ApoA2).
    • Source: Typically due to genetic mutations in the APOA1 and APOA2 genes.
  5. Gelsolin Amyloidosis:
    • Abnormal Protein: Gelsolin.
    • Source: Due to mutations in the GSN gene.
  6. Lysozyme Amyloidosis:
    • Abnormal Protein: Lysozyme.
    • Source: Due to mutations in the LYz gene.
  7. Fibrinogen Aα Chain Amyloidosis:
    • Abnormal Protein: Fibrinogen Aα chain.
    • Source: Due to mutations in the FGA gene.
  8. Cystatin C Amyloidosis:
    • Abnormal Protein: Cystatin C.
    • Source: Due to mutations in the CST3 gene.
  9. Beta-2 Microglobulin (β2M) Amyloidosis:
    • Abnormal Protein: Beta-2 microglobulin.
    • Source: Seen in patients on long-term dialysis and those with certain blood disorders.
These are just a few examples of the many types of amyloidosis, each associated with specific abnormal proteins.

I wonder if all LC patients have to have muscle biopsies. Or would they present special blood tests, or will they use the already-known DNA as a biomarker?

Amyloid deposits in skeletal muscle can be associated with various illnesses and conditions. These deposits can affect muscle function and lead to a range of symptoms.

Another wait-and-see and more waiting for peer reviews.
 
Last edited:

hapl808

Senior Member
Messages
2,181
The problem with a lot of these 'abnormalities' is you need to test against healthy people, and against people with other illnesses. That will help also determine if these things are just downstream effects of poor health, or unique or causal.
 

Violeta

Senior Member
Messages
3,014
Endoplasmic reticulum (ER) is involved in the processing and trafficking of amyloid precursor protein (APP).

Yes, this study is about amyloid in the brain. But I think I saw something yesterday about amyloid in the muscle, if I can find it again I'll bring it here.

The role of endoplasmic reticulum in amyloid precursor protein processing and trafficking: Implications for Alzheimer's disease​


https://www.sciencedirect.com/scien...is involved,endoplasmic reticulum (ER) stress.
 

Violeta

Senior Member
Messages
3,014
Here's a clue from someone on Twitter, if anyone's brain is up to it this evening.

"Or perhaps due to breakdown of the ubiquitin-proteasome system?"

Ubiquitin-proteasome system has an immense impact on the amyloidogenic pathway of amyloid precursor protein (APP) processing that generates Abeta....
 
Back