Amyloidosis Induced By The Sars-CoV-2 Spike Protein: The Fibrils Are Not Nanotechnology or Graphene Oxide

May 22, 2022

This is all related to Prions. Initially, in late spring of 2020, I thought the SARS-CoV-2 Spike Protein was an aerosolized Prion. However, it is actually far more insidious. It is an Aerosolized Toxic Oligomer.


What are we observing, then?

The protein fibrils forming in association with Alzheimer’s, Parkinson’s and Type II Diabetes (misfolded aggregates) share common properties such as a core rich in β-sheet structure adopting a characteristic cross-β topology, the resistance to degradation and significant mechanical properties with TENSILE STRENGTH THAT IS SIMILAR TO STEEL. This strength has been previously confused with graphene oxide.

The recent paper out of Sweden noted the “perfect” form of the Amyloid Fibrils induced by the Spike Protein. These formations have been previously confused with nanotechnology.

But how does this occur? What is the mechanism?

The structural similarity between the mature amyloid aggregates in these misfolding diseases has suggested the existence of some generic mechanism of toxicity. And, the SPIKE PROTEIN BINDS TO ALL AMYLOIDIC CELLS IN THE BODY.

The heparin binding and aggregation propensity of S1 protein has been suggested the ability of S1 to form amyloid and toxic aggregates that can act as seeds to aggregate many of the misfolded brain proteins and can ultimately leads to neurodegeneration. It has been suggested that SARS-CoV-2 infection invades the CNS by controlling protein synthesis machinery, disturbs endoplasmic reticulum and mitochondrial function and increases the accumulation of misfolded proteins, thereby activates protein aggregation, mitochondrial oxidative stress, apoptosis and neurodegeneration.

IT IS THE CLEAVED SPIKE PROTEIN THAT INDUCES SYSTEMIC AMYLOIDOSIS. I believe that the Spike Proteins generated by both infection and vaccination are cleaved. Flooding the body with S1 subunits seeding the body with misfolded amyloids.

Which brings us to the phenomenon of de novo onset of Type II Diabetes post COVID (and, I believe there are reports post vaccination).

And this is the point:

Young rodents that had been genetically modified to crank out human (islet amyloid polypeptide) IAPP are normally healthy, but when the scientists injected them with synthetic IAPP or with material from the pancreases of diabetic mice, IAPP conglomerations formed in the pancreas. As with prions, a smidgen of misfolded IAPP acts like a seed that spurs new clusters of the abnormal protein to grow.

Are we not injecting humans with a misfolding amyloidic protein?

Referenced/Related Papers

SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration

Membrane Interactions and Toxicity by Misfolded Protein Oligomers

Could diabetes spread like mad cow disease?