October 16, 2021
A NOVEL PROTEINOPATHY: ALZHEIMER’S, ALS, HUNTINGTON’S, PARKINSON’S AND PRION DISEASE ALL HAVE ONE COMMON PATHOGENIC TRAIT: THEY ALL RESULT FROM THE AGGREGATION OF PROTEINS
THE SPIKE PROTEIN MAY COMBINE IN A MIX/MATCH FASHION TO “CUSTOM TAILOR” NEURODEGENERATION IN THE HOST
When you hear of neurodegenerative disease, you think of “brain eating” disorders. That’s not really the case. The damage to the brain and CNS is caused by an abundance of misfolded proteins, which appears to be toxic to cells, leading to their injury and death. A disease's severity often correlates with the expression levels of the protein. The toxic accumulation occurs in different parts of the brain and can be in the nucleus, cytoplasm, or extracellular space.
The spike protein is itself a prion domain (a type of misfolded protein which can aggregate). It has been observed to bind (aggregate) the kind of proteins found in Alzheimer’s Disease. In summary, the findings reported in a study from May support the hypothesis that the SARS-CoV-2 spike protein can interact with heparin binding amyloid forming proteins.
The Spike Protein has also been shown to bind to receptors which induce Parkinson’s Disease.
The Spike Protein also has Prion-Like domains.
It is very possible, that given the Spike Protein’s ability to travel in exosomes, that it may bind with/amplify any preexisting proteinopathy. It may also induce a de novo proteinopathy in a previously healthy host.
Investigations into this probably mechanism must be conducted ASAP.
Prions are “indestructible.” Is the Spike Protein, as well? The S1 unit has been found in monocytes 15 months post infection.
SARS-CoV-2 spike protein interactions with amyloidogenic proteins: Potential clues to neurodegeneration
SARS-CoV-2 Prion-Like Domains in Spike Proteins Enable Higher Affinity to ACE2
Possible Link between SARS-CoV-2 Infection and Parkinson’s Disease: The Role of Toll-Like Receptor 4
SARS-CoV-2 nucleoprotein can trigger α-synuclein amyloid fibril formation