SEVERE COVID, LONG COVID AND SPIKE-PROTEIN INDUCED SYSTEMIC AMYLOIDOSIS AS AN AUTOCATALYTIC REACTION: IT IS NOT A QUESTION OF AMYLOID OR PRION, IT IS DEPENDENT ON THE RATE OF PROTEIN AUTOCATALYSIS AND
SEVERE COVID, LONG COVID AND SPIKE-PROTEIN INDUCED SYSTEMIC AMYLOIDOSIS AS AN AUTOCATALYTIC REACTION: IT IS NOT A QUESTION OF AMYLOID OR PRION, IT IS DEPENDENT ON THE RATE OF PROTEIN AUTOCATALYSIS AND
SEVERE COVID, LONG COVID AND SPIKE-PROTEIN INDUCED SYSTEMIC AMYLOIDOSIS AS AN AUTOCATALYTIC REACTION: IT IS NOT A QUESTION OF AMYLOID OR PRION, IT IS DEPENDENT ON THE RATE OF PROTEIN AUTOCATALYSIS AND
“Misfolded PrP was amplified by rounds of sonication…” Sonification - really. Now that’s interesting. Based on the way it’s referred to in the excerpt, I gather it’s a standard technique in this sort of research.
I find it particularly interesting in relation to the accelerating blanketing of our planet with radio waves/EMFs. The energy of which I assume have sound components outside the audible spectrum.
In Sweden they are using low level laser therapy and also infrared light therapy to slow and/or reverse the amyloids. Also, Danish biotechnology firm QuantBioRes is testing deactivation mechanism for Covid. They have been using Resonant Recognition Model (RRM) technology to predict bioactive mutations and electromagnetic frequency, among other markers, and study protein activity with the goal to produce treatments for resistant bacteria and viral diseases. What they are finding could be used in reversing dementia like processes. How do I know all this? I tried everything I could to help my mum when she was diagnosed with dementia. We visited so many research centres, universities, neurologist, nutritionists etc and tried everything we were told…
I can not help but wonder, what would happen if Walter and all the other brilliant scientist active here on substack and Twitter were to join their brain power to find some sort of cure for Covid/Dementia? What would need to happen to get you all on board? What is the amount of $$$ that would make that possible? Who would you like to be a Project Lead? How would you like to work with? What would you need to happen to collaborate? What is stopping you? What would be one thing that would motivate you to join your brain power and work together on cure for Covid/Dementia?
Your work has synergies with research that is going on at University of Tasmania
I am not sure what is the best way to connect so I am sharing their details. James is the admin officer there, Professor James Vickers is a Director and both would be happy to engage with you and/or look into possible co-research projects
There are some glycine zipper epitopes in the spike protein at the c-terminal end. Look for the GFIAGLIAIVM (L instead of M in SARS1). There are also two GxxxG peptides in the "lower heads" of the spike (GWIFG, GWTAG and GCLIG). This is background https://www.frontiersin.org/articles/10.3389/fnagi.2016.00107/full
Thanks again Walter, brilliant, love you analysis. I’ve always wondered how they will explain away the coming catastrophe. Has a narrative been created that the virus will do this by mutating. I’m just thinking outside the box. Geert has predicted this, but steered clear of criticising the vaccines
The occurrence of hyperactivated platelets and fibrinaloid microclots in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
Massimo Nunes, Arneaux Kruger, Amy Proal, Douglas Kell, Etheresia Pretorius
Abstract We have previously demonstrated that platelet poor plasma (PPP) obtained from patients with LongCovid/Post-Acute Sequelae of COVID-19 (PASC) is characterized by a hypercoagulable state reflected in hyperactivated platelets and the presence of considerable numbers of fibrin(ogen) amyloid microclots or fibrinaloid microclots. Due to substantial overlap in symptoms and aetiology between PASC and ME/CFS, we investigated whether coagulopathies, platelet hyperactivation and/or fibrin amyloid formation differed between individuals exhibiting ME/CFS and gender- and age-matched healthy controls. ME/CFS patients were statistically far more hypercoagulable as judged by thromboelastography of both whole blood and platelet-poor plasma. The area of plasma images containing fibrinaloid microclots was commonly more than 10-fold greater in untreated platelet-poor plasma from individuals with ME/CFS than in that of healthy controls.
One of these drugs is tacrolimus. Didn't Adam Gaertner recommend this last year? The others are ninedanib (Ofev), a TKI for lung fibrotic disease, and zotafin, a chemo drug which blocks growth in TKI driven tumers.
What do they have in common? anti- fibrotic or potentially anti-fibrotic?
And didn't Walter Chesnut write about Covid and fibrosis?
The responses had to do with big pharma and how much they would try to make off these drugs. gutwat thinks they may be able to slow it down but isn't sure this is a cure.
My 35 year old niece appears to have developed POTS. Could this be amyloid/spike protein related? She got 2 Pfizer shots and may have had covid subsequently. Her life is over if we can't fix this. Thanks.
SEVERE COVID, LONG COVID AND SPIKE-PROTEIN INDUCED SYSTEMIC AMYLOIDOSIS AS AN AUTOCATALYTIC REACTION: IT IS NOT A QUESTION OF AMYLOID OR PRION, IT IS DEPENDENT ON THE RATE OF PROTEIN AUTOCATALYSIS AND
“Misfolded PrP was amplified by rounds of sonication…” Sonification - really. Now that’s interesting. Based on the way it’s referred to in the excerpt, I gather it’s a standard technique in this sort of research.
I find it particularly interesting in relation to the accelerating blanketing of our planet with radio waves/EMFs. The energy of which I assume have sound components outside the audible spectrum.
Is there a lab test that one could order, or do, that would answer a question whether one is affected by the amyloids described? Thanks
Lumbrokinase nattokinase
Great insights Walter.
In Sweden they are using low level laser therapy and also infrared light therapy to slow and/or reverse the amyloids. Also, Danish biotechnology firm QuantBioRes is testing deactivation mechanism for Covid. They have been using Resonant Recognition Model (RRM) technology to predict bioactive mutations and electromagnetic frequency, among other markers, and study protein activity with the goal to produce treatments for resistant bacteria and viral diseases. What they are finding could be used in reversing dementia like processes. How do I know all this? I tried everything I could to help my mum when she was diagnosed with dementia. We visited so many research centres, universities, neurologist, nutritionists etc and tried everything we were told…
I can not help but wonder, what would happen if Walter and all the other brilliant scientist active here on substack and Twitter were to join their brain power to find some sort of cure for Covid/Dementia? What would need to happen to get you all on board? What is the amount of $$$ that would make that possible? Who would you like to be a Project Lead? How would you like to work with? What would you need to happen to collaborate? What is stopping you? What would be one thing that would motivate you to join your brain power and work together on cure for Covid/Dementia?
Dear Walter
Your work has synergies with research that is going on at University of Tasmania
I am not sure what is the best way to connect so I am sharing their details. James is the admin officer there, Professor James Vickers is a Director and both would be happy to engage with you and/or look into possible co-research projects
dementia.care@utas.edu.au.
James Jestrimski Phone: + 61 3 62266912
Administration Officer
Wicking Dementia Research and Education Centre
University of Tasmania – Private Bag 143, Hobart TAS 7001
utas.edu.au
Horror show.
The death & damage from the DEATHVAX™ continues to pile up...
https://2ndsmartestguyintheworld.substack.com/p/two-new-studies-show-link-between?s=w
There are some glycine zipper epitopes in the spike protein at the c-terminal end. Look for the GFIAGLIAIVM (L instead of M in SARS1). There are also two GxxxG peptides in the "lower heads" of the spike (GWIFG, GWTAG and GCLIG). This is background https://www.frontiersin.org/articles/10.3389/fnagi.2016.00107/full
Thanks again Walter, brilliant, love you analysis. I’ve always wondered how they will explain away the coming catastrophe. Has a narrative been created that the virus will do this by mutating. I’m just thinking outside the box. Geert has predicted this, but steered clear of criticising the vaccines
Wow. Thank you, Igor.
I ran into this paper in this article. Quite a nice breakthrough: https://www.news-medical.net/news/20200506/New-breakthrough-may-help-cure-prion-disease.aspx
And a couple months ago I ran into Artemisinen: https://www.sciencedirect.com/science/article/pii/S221323171730099X?via%3Dihub
Lumbrokinase. Therapeutics found!
"Prioloid. Love it!
PREPRINT EXCERPT Fibrinaloid microclots in ME/CFS, too
https://www.researchsquare.com/article/rs-1727226/v1
The occurrence of hyperactivated platelets and fibrinaloid microclots in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
Massimo Nunes, Arneaux Kruger, Amy Proal, Douglas Kell, Etheresia Pretorius
Abstract We have previously demonstrated that platelet poor plasma (PPP) obtained from patients with LongCovid/Post-Acute Sequelae of COVID-19 (PASC) is characterized by a hypercoagulable state reflected in hyperactivated platelets and the presence of considerable numbers of fibrin(ogen) amyloid microclots or fibrinaloid microclots. Due to substantial overlap in symptoms and aetiology between PASC and ME/CFS, we investigated whether coagulopathies, platelet hyperactivation and/or fibrin amyloid formation differed between individuals exhibiting ME/CFS and gender- and age-matched healthy controls. ME/CFS patients were statistically far more hypercoagulable as judged by thromboelastography of both whole blood and platelet-poor plasma. The area of plasma images containing fibrinaloid microclots was commonly more than 10-fold greater in untreated platelet-poor plasma from individuals with ME/CFS than in that of healthy controls.
@gutwat1 posted this on twitter the AM. Thought it might interest you. I have her permission to copy to you.
science.org/DOI/10.1126/sciadv.abm2510
One of these drugs is tacrolimus. Didn't Adam Gaertner recommend this last year? The others are ninedanib (Ofev), a TKI for lung fibrotic disease, and zotafin, a chemo drug which blocks growth in TKI driven tumers.
What do they have in common? anti- fibrotic or potentially anti-fibrotic?
And didn't Walter Chesnut write about Covid and fibrosis?
The responses had to do with big pharma and how much they would try to make off these drugs. gutwat thinks they may be able to slow it down but isn't sure this is a cure.
My 35 year old niece appears to have developed POTS. Could this be amyloid/spike protein related? She got 2 Pfizer shots and may have had covid subsequently. Her life is over if we can't fix this. Thanks.
Quercetin for amyloids and the prion subclass
Thank you Walter! I guess you’ve already identified this article https://portlandpress.com/biochemj/article/479/4/537/230829/A-central-role-for-amyloid-fibrin-microclots-in