Understanding Prior History Of Covid19 And C19 Vaccination Association With Amyloid Fibril Production and Prion Disease - Rationale For Methylene Blue - Literature Review

Ana Maria Mihalcea, MD, PhD - Dec 16, 2023 ∙ Paid ∙ Source

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In this follow up article, I want to explain the background information of the association of Covid19 prior infection, the C19 bioweapon shots and the production of amyloid and prions. In previous posts, I explained the assocation with self assembly nanotechnology. I also described the scientifically documented usefulness of Methylene Blue as a therapeutic option. Here I will review the literature, that correlates Sars Cov 2 infection and C19 injectable bioweapon side effects with amyloidosis and prion disease. Other prominent scientists have spoken about this association, for example Jessica Rose:

Modified spike protein RNA injection-induced Amyloidosis?

I don't think it's Myocarditis, I think it's injection-induced Cardiac Amyloidosis

A paper published in 2017 provides some compelling evidence for the SARS nCoV-2 spike-amyloid theory

I have posted the Russian study that showed that the Amyloid realted to SARS Cov2 ARE SELF ASSEMBLY NANOPARTICLES AND NANOFIBERS:

There was a Nature paper that discussed that the SYNTHETIC PROTEINS MADE ( you can also call that self assembly nanotechnology hydrogels since it is a synthetic process), are Amyloid fibrils.

Amyloidogenesis of SARS-CoV-2 Spike Protein

SARS-CoV-2 infection is associated with a surprising number of morbidities. Uncanny similarities with amyloid-disease associated blood coagulation and fibrinolytic disturbances together with neurologic and cardiac problems led us to investigate the amyloidogenicity of the SARS-CoV-2 spike protein (S-protein). Amyloid fibril assays of peptide library mixtures and theoretical predictions identified seven amyloidogenic sequences within the S-protein. All seven peptides in isolation formed aggregates during incubation at 37 °C. Three 20-amino acid long synthetic spike peptides (sequence 192–211, 601–620, 1166–1185) fulfilled three amyloid fibril criteria: nucleation dependent polymerization kinetics by ThT, Congo red positivity, and ultrastructural fibrillar morphology. Full-length folded S-protein did not form amyloid fibrils, but amyloid-like fibrils with evident branching were formed during 24 h of S-protein coincubation with the protease neutrophil elastase (NE) in vitro . NE efficiently cleaved S-protein, rendering exposure of amyloidogenic segments and accumulation of the amyloidogenic peptide 194–203, part of the most amyloidogenic synthetic spike peptide. NE is overexpressed at inflamed sites of viral infection. Our data propose a molecular mechanism for potential amyloidogenesis of SARS-CoV-2 S-protein in humans facilitated by endoproteolysis. The prospective of S-protein amyloidogenesis in COVID-19 disease associated pathogenesis can be important in understanding the disease and long COVID-19.

Amyloidosis is the deposition of these fibrills that cannot be dissolved by conventional blood thinners in the body. I have seen cases like this of rapid fatal amyloidosis in a patient exposed to C19 vaccine shedding.

Understanding SARS-CoV-2-induced systemic amyloidosis

The team discovered seven synthetic (amyloidogenic) peptides which were 20 amino acids in length within the S protein and found that six of them were in beta-sheet conformation as observed in the cryo-EM structure of SARS-CoV-2 S protein in its closed state. It was noted that these peptides in isolation could aggregate as fibrils at 37°C during incubation. Of these seven peptides, three peptides were found to meet the criteria of amyloid fibrils

These fibrils or what I call self assembly nanotechnology hydrogels cause neurological symptoms and clots.

Misfolded spike protein could explain complicated COVID-19 symptoms

SARS-CoV-2, the virus that causes COVID-19, can produce short-term and long-term symptoms. Researchers of a new study found that amyloids, the abnormal proteins that are also known to cause Alzheimer’s, could be formed during SARS-CoV-2 infection, which could explain some of the symptoms experienced. The research suggests that the immune system’s interaction with SARS-CoV-2 may be leading to the production of these misfolded spike proteins, resulting in blood clots and neurological symptoms.

The same amyloid fibrills also cause neurotoxicity:

Neurotoxic amyloidogenic peptides in the proteome of SARS-COV2: potential implications for neurological symptoms in COVID-19

COVID-19 is primarily known as a respiratory disease caused by SARS-CoV-2. However, neurological symptoms such as memory loss, sensory confusion, severe headaches, and even stroke are reported in up to 30% of cases and can persist even after the infection is over (long COVID). These neurological symptoms are thought to be produced by the virus infecting the central nervous system, however we don’t understand the molecular mechanisms triggering them. The neurological effects of COVID-19 share similarities to neurodegenerative diseases in which the presence of cytotoxic aggregated amyloid protein or peptides is a common feature. Following the hypothesis that some neurological symptoms of COVID-19 may also follow an amyloid etiology we identified two peptides from the SARS-CoV-2 proteome that self-assemble into amyloid assemblies. Furthermore, these amyloids were shown to be highly toxic to neuronal cells. We suggest that cytotoxic aggregates of SARS-CoV-2 proteins may trigger neurological symptoms in COVID-19.

Of note, Prion disease, which is a similar protein misfolding also has been on the rise.

Prion Disease Rising in the U.S.

The incidence of Creutzfeldt-Jakob disease (CJD), a universally fatal prion disease that progresses rapidly, rose consistently from 2007 to 2020, a study of death certificates showed.

More evidence of the infection and post vaccination Amyloidosis:

COVID-19 Infection and Vaccination and Its Relation to Amyloidosis: What Do We Know Currently?

Amyloidosis is a complex disorder characterized by deposited insoluble fibrillar proteins which misfold into β-pleated sheets. The pathogenesis of amyloidosis can vary but can be the result of immune dysregulation that occurs from sustained high inflammatory states, often known as AA amyloidosis. Multi-organ involvement including hepatic, gastrointestinal, renal, cardiac and immunological pathological manifestations has been observed amongst individuals presenting with amyloidosis. The recent global pandemic of severe acute respiratory syndrome coronavirus 2, also referred to as coronavirus 2019 (COVID-19), has been shown to be associated with multiple health complications, many of which are similar to those seen in amyloidosis. Though COVID-19 is recognized primarily as a respiratory disease, it has since been found to have a range of extra-pulmonary manifestations, many of which are observed in patients with amyloidosis. These include features of oxidative stress, chronic inflammation and thrombotic risks. It is well known that viral illnesses have been associated with the triggering of autoimmune conditions of which amyloidosis is no different. Over the recent months, reports of new-onset and relapsed disease following COVID-19 infection and vaccination have been published.

Further evidence that Amyloid processing is associated with neurological symptoms.

Amyloid processing in COVID-19-associated neurological syndromes

SARS-CoV-2 infection can damage the nervous system with multiple neurological manifestations described. However, there is limited understanding of the mechanisms underlying COVID-19 neurological injury. This pilot study raises the possibility that patients with COVID-19-associated neurological syndromes exhibit impaired amyloid processing. Altered amyloid processing was linked to neuronal injury and neuroinflammation but reduced astrocyte activation.

Prion disease has been reported after C19 synthetic bioweapon exposure

Prion Disease After COVID-19: A Case Report

Our case demonstrates the potential correlation of COVID with neurodegenerative conditions, especially prion disorders.

Here is another case report of rapid neurological degeneration - I have seen cases in my clinic with severe neurological impairment and have been able to reverse them with the treatments I have been discussing in my substack.

Creutzfeldt-Jakob disease after COVID-19: infection-induced prion protein misfolding? A case report

Creutzfeldt-Jakob disease (CJD) is a rare, fatal disease presenting with rapidly progressive neurological deficits caused by the accumulation of a misfolded form (PrPSc) of prion protein (PrPc). Coronavirus disease 2019 (COVID-19) is a primarily respiratory syndrome caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); many diverse neurological complications have been observed after COVID-19.

We describe a young patient developing CJD two months after mild COVID-19. Presenting symptoms were visuospatial deficits and ataxia, evolving into a bedridden state with preserved consciousness and diffuse myoclonus. Diagnostic work-up was suggestive of CJD. The early age of onset and the short interval between respiratory and neurological symptoms might suggest a causal relationship: a COVID-19-related neuroinflammatory state may have induced the misfolding and subsequent aggregation of PrPSc. The present case emphasizes the link between neuroinflammation and protein misfolding.

Here is further evidence:

COVID-19 and Neurodegenerative Diseases: Prion-Like Spread and Long-Term Consequences

…the potential acceleration of prion-like proteins spread following SARS-CoV-2 infection.

I have discussed the correlations of the Amyloid and Prion protein in Nanotechnology hydrogel, which would also explain the weaponization of the self assembly amyloid process as a depopulation weapon as well as a substrate for surveillance technology.

Whatever you believe or don’t believe, if you want to talk about Amyloids and Prions or the implication in nanotechnology self assembly, either way, Methylene Blue provides a well researched scientifically recognized method of reversing this problem, hence should be considered by everyone.

I hope this methodical explanation helped. One of the problems from this bioweapon assault is amyloids and prions, that can cause heart disease, blood clots and neurological decline and Methylene Blue helps disolve these misfolded proteins.

Methylene Blue is available over the counter or in compounded form. Dosages may vary individually from 10-20 mg or 50 mg as I recommend for most adults. MB is contraindicated if you take serotonin reuptake inhibitor antidepressants.

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