When I first saw this story I thought “Looks like Click Bait or maybe Paranoid Fantasy”.
Digging into it a bit, it now looks like the guy’s basic science is right, and his concerns have some merit. There’s still way too many “could” and “might” and maybe type qualifiers in the article, and it is in an “also ran” type “journal”. Yet his claims about other diseases (that was part of my dismissal) have in fact checked out.
In The News
“Popular Press” version:
Report: Pfizer and Moderna COVID “Vaccines” Could Trigger Alzheimer’s, ALS, and Other Neurological Degenerative Diseases
By Jim Hoft
Published April 25, 2021 at 1:53pm
Everyone from Joe Biden to Red Pope Francis is pushing for 100% acceptance of the mRNA vaccine for COVID. The vaccine is unproven and untested. No one knows if the vaccine is more dangerous than the disease.
Over 50 percent of new COVID cases involve people who have already been vaccinated, [as reported on The Gateway Pundit earlier, according to a Yale epidemiologist]).
Now, a startling new report in *Microbiology and Infectious Disease* finds the mRNA vaccines could trigger Alzheimer’s disease, ALS, and other neurological and cognitive degenerative diseases.
Dr. Classen and his associates found that the vaccine increases the likelihood of these hideous diseases by opening a pathway into human DNA, which is exactly what this gene-therapy drug is intended to do:
The results indicate that the vaccine RNA has specific sequences that may induce TDP-43 and FUS to fold into their pathologic prion confirmations. In the current analysis a total of sixteen UG tandem repeats (ΨGΨG) were identified and additional UG (ΨG) rich sequences were identified. Two GGΨA sequences were found. Potential G Quadruplex sequences are possibly present but a more sophisticated computer program is needed to verify these. Furthermore, the spike protein, created by the translation of the vaccine RNA, binds angiotensin converting enzyme 2 (ACE2), a zinc containing enzyme.
The “Greek pitchfork” psi letter is intended to mean a variant form of U Uracil named 1-methyl-3′-pseudouridylyl used in the vaccine for God Only Knows why.
It goes on from there into the supposed risk of more zinc inside the cells:
More about that issue with zinc:
This interaction has the potential to increase intracellular zinc. Zinc ions have been shown to cause the transformation of TDP-43 to its pathologic prion configuration. The folding of TDP-43 and FUS into their pathologic prion confirmations is known to cause ALS, front temporal lobar degeneration, Alzheimer’s disease and other neurological degenerative diseases.
Since Zinc is essential to several dozen enzyme systems and is increased via drugs like HCQ / Quinine / Quercitin to help prevent viral replication, I’m a bit sceptical of that claim and would like to know if this was found via an in vitro test with massive zinc… but I digress.
Going down the Rabbit Hole:
Here’s the PDF of the report:
https://www.hennessysview.com/images/covid19-rna-based-vaccines-and-the-risk-of-prion-disease-1503.pdf All of 3 pages long, full of maybes of various kinds.
COVID-19 RNA Based Vaccines and the Risk of Prion Disease
Classen Immunotherapies, Inc., 3637 Rockdale Road, Manchester,
MD 21102, E-mail: email@example.com.
J. Bart Classen, MD*
Citation: Classen JB. COVID-19 RNA Based Vaccines and the Risk of Prion Disease. Microbiol Infect Dis. 2021; 5(1): 1-3.
Development of new vaccine technology has been plagued with problems in the past. The current RNA based SARSCoV-2 vaccines were approved in the US using an emergency order without extensive long term safety testing. In this paper the Pfizer COVID-19 vaccine was evaluated for the potential to induce prion-based disease in vaccine recipients. The RNA sequence of the vaccine as well as the spike protein target interaction were analyzed for the potential to convert intracellular RNA binding proteins TAR DNA binding protein (TDP-43) and Fused in Sarcoma (FUS) into their pathologic prion conformations. The results indicate that the vaccine RNA has specific sequences that may induce TDP-43 and FUS to fold into their pathologic prion confirmations. In the current analysis a total of sixteen UG tandem repeats (ΨGΨG) were identified and additional UG (ΨG) rich sequences were identified. Two GGΨA sequences were found. Potential G Quadruplex sequences are possibly present but a more sophisticated computer program is needed to verify these. Furthermore, the spike protein, created by the translation of the vaccine RNA, binds angiotensin converting enzyme 2 (ACE2), a zinc containing enzyme. This interaction has the potential to increase intracellular zinc. Zinc ions have been shown to cause the transformation of TDP-43 to its pathologic prion configuration. The folding of TDP-43 and FUS into their pathologic prion confirmations is known to cause ALS, front temporal lobar degeneration, Alzheimer’s disease and other neurological degenerative diseases. The enclosed finding as well as additional potential risks leads the author to believe that regulatory approval of the RNA based vaccines for SARS-CoV-2 was premature and that the vaccine may cause much more harm than benefit.
Pfizer’s RNA based vaccine against COVID-19 was evaluated for the potential to convert TDP-43 and or FUS to their prion based disease causing states. The vaccine RNA was analyzed for the presence of sequences that can activate TDP-43 and FUS. The interaction of the transcribed spike protein with its target was analyzed to determine if this action could also activate TDP-43 and FUS.
So basically they loooked at the vaccine RNA looking for sequences similar to those that create protein segments that cause mis-folding of proteins in other Prion diseases. OK… So not a smoking gun, not even a gunshot victim. Just saying “does it look like the outline of a gun?”…
Weak tea. OTOH, you can’t exactly go around injecting an experimental RNA segment into people and creating an experimental spike protein fragment to find out IF in fact it will screw up their brains in a decade or two. Oh. Wait…
Analysis of the Pfizer vaccine against COVID-19 identified two potential risk factors for inducing prion disease is humans. The RNA sequence in the vaccine  contains sequences believed to induce TDP-43 and FUS to aggregate in their prion based conformation leading to the development of common neurodegerative diseases. In particular it has been shown that RNA sequences GGUA , UG rich sequences , UG tandem repeats , and G Quadruplex sequences , have increased affinity to bind TDP-43 and or FUS and may cause TDP-43 or FUS to take their pathologic configurations in the cytoplasm. In the current analysis a total of sixteen UG tandem repeats (ΨGΨG) were identified and additional UG (ΨG) rich sequences were identified. Two GGΨA sequences were found. G Quadruplex sequences are possibly present but sophisticated computer programs are needed to verify these. The spike protein encoded by the vaccine binds angiotensin converting enzyme 2 (ACE2), an enzyme which contains zinc molecules . The binding of spike protein to ACE2 has the potential to release the zinc molecule, an ion that causes TDP-43 to assume its pathologic prion transformation .
Now at this point I was thinking “WT?” as I only knew of ONE Prion Disease, the spongiform encephalitis one. Kuro or CJV / vCJV in humans, Mad Cow in cows, Scrapie in sheep, Chronic Wasting Disease in deer. All caused by a misfold of the same PrP protein.
Down below you will find where I went down that Rabbit Hole and found that yes, his claims of Alzheimers, ALS, and others being prion diseases is correct. That’s a real thing.
Skipping down in the paper, he gets a bit paranoid … OTOH, we now know our Dear Leaders are largely Sociopathic Liars For Effect and have a death wish for 90% of the world population, so maybe “just because you are paranoid doesn’t mean they aren’t out to get you” applies…
Over the last two decades there has been a concern among certain scientists that prions could be used as bioweapons. More recently there has been a concern that ubiquitous intracellular molecules could be activated to cause prion disease including Alzheimer’s disease, ALS and other neurodegenerative diseases. This concern originates due to potential for misuse of research data on the mechanisms by which certain RNA binding proteins like TDP-43, FUS and others can be activated to form disease causing prions. The fact that this research, which could be used for bioweapons development, is funded by private organizations including the Bill and Melinda Gates Foundation, and Ellison Medical Foundation  without national/international oversight is also a concern.
Jumping on down to the Zink part of the paper:
Zinc binding to the RNA recognition motif of TDP-43 is another mechanism leading to formation of amyloid like aggregations . The viral spike protein, coded by the vaccine RNA sequence, binds ACE2 an enzyme containing zinc molecules . This interaction has the potential to increase intracellular zinc levels leading to prion disease. The initial binding could be between spike proteins on the surface of the cell transfected by the vaccine and ACE2 on the surface of an adjacent cell. The resulting complex may become internalized. Alternatively, the interaction could initially take place in the cytoplasm of a cell that makes ACE2 and has been transfected with the vaccine RNA coding for the spike protein. The interaction is quite concerning given the belief that the virus causing COVID-19, SARS-CoV-2, is a bioweapon [10,11] and it is possible that the viral spike protein may have been designed to cause prion disease.
I would like to know more about just how much zinc it takes and in what context. Being essential to so many functions, I have difficulty with the idea that normal levels of zink can be damaging…
Then we have the Why Psi issue:
Another related concern is that the Pfizer vaccine uses a unique RNA nucleoside 1-methyl-3′-pseudouridylyl (Ψ). According to FDA briefing documents, this nucleoside was chosen to reduce activation of the innate immune system . RNA molecules containing this nucleoside will undoubtedly have altered binding . Unfortunately, the effect on TDP-43, FUS and other RNA binding proteins is not published. The use of this nucleoside in a vaccine can potentially enhance the binding affinity of RNA sequences capable of causing TDP-43 and FUS to assume toxic configurations.
Skipping over some more, he makes an interesting citation that bears investigation, and then returns a to a bit more paranoid context (which I will ommitt this time):
Finally, others working in the field have published additional support that COVID-19 vaccines could potentially induce prion disease. Authors  found prion related sequences in the COVID-19 spike protein which were not found in related coronaviruses. Others  have reported a case of prion disease, Creutzfeldt-Jakob disease, initially occurring in a man with COVID-19.
So looks like Chinese Wuhan Covid itself might cause the issues too. Sort of a damned if you do, damned if you don’t. I think I’m sticking with Ivermectin…
Do realize that there is genetic variation in the related prion-potential protein formation and it is highly likely some few folks will be extraordinarily predisposed while others will be extraordinarily resistant. So YMMV…
J. Bart Classen, MD, Classen Immunotherapies, Inc., 3637
Rockdale Road, Manchester, MD 21102, Tel: 410-377-8526.
Received: 27 December 2020; Accepted: 18 January 2021
Microbiology & Infectious Diseases
COVID-19, Vaccines, Diabetes, Immunity
OK, other bits
Background on what’s a Prion. Looks correct to me. Also includes references to other Prion diseases that I’d not noticed had been worked out. Progress and all that…
In other diseases
Prion-like domains have been found in a variety of other mammalian proteins. Some of these proteins have been implicated in the ontogeny of age-related neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U), Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. They are also implicated in some forms of systemic amyloidosis including AA amyloidosis that develops in humans and animals with inflammatory and infectious diseases such as tuberculosis, Crohn’s disease, rheumatoid arthritis, and HIV AIDS. AA amyloidosis, like prion disease, may be transmissible. This has given rise to the ‘prion paradigm’, where otherwise harmless proteins can be converted to a pathogenic form by a small number of misfolded, nucleating proteins.
Even a proposed treatment for such diseases via modulating the genes that code for the protein in question (assuming one can live with it turned off):
So looks like we’re starting to have a handle on things like Alzheimers and Parkinson’s. Which makes this a bit more believable:
Has en embedded video of folks with Parkinson’s like symptoms with onset just after vaccination… IMHO, vaccines kill off the folks with variant genetics just a little too far removed from the study group. ( I knew a person in a wheelchair for life after a Polio vaccination… her twin brother did fine.)
Bitchute Channel, Sixth Sense, 32:26 Minute Video
“One of the symptoms of prion disease is muscle control loss, sudden jerks or twitches, exactly the adverse effect many are experiencing. And, we have heard from Bill Gates, and other ‘experts’ that another pandemic is coming, which will be a virus that will be far more deadly. Based on the study highlighted in this video, it may very well be that the Covid-19 vaccine will make the vaccinated far more susceptible to dying.”
Two COVID vaccinated people suffering from uncontrollable body convulsions:
Those two names being links in the article. So maybe it’s only a few dozen out of millions… Maybe It’s OK to sacrifice a few dozens, or hundreds, to the Gods Of CDC. Or maybe it ought to be more informed consent with “reparations” to the damaged families via liability, and maybe we need to wonder if there’s a Long Term Slow Onset form too…
I also got confirmation of some of the claims about other diseases too:
Handbook of Clinical Neurology
Volume 153, 2018, Pages 337-354
Chapter 18 – Prion-like mechanisms in amyotrophic lateral sclerosis
Author Jacob I.Ayers 1 Neil R.Cashman 2
The prion hypothesis – a protein conformation capable of replicating without a nucleic acid genome – was heretical at the time of its discovery. However, the characteristics of the disease-misfolded prion protein and its ability to transmit disease, replicate, and spread are now widely accepted throughout the scientific community. In fact, in the last decade a wealth of evidence has emerged supporting similar properties observed for many of the misfolded proteins implicated in other neurodegenerative diseases, such as Alzheimer disease, Parkinson disease, tauopathies, and as described in this chapter, amyotrophic lateral sclerosis (ALS). Multiple studies have now demonstrated the ability for superoxide dismutase-1, 43-kDa transactive response (TAR) DNA-binding protein, fused-in sarcoma, and most recently, C9orf72-encoded polypeptides to display properties similar to those of prions. The majority of these are cell-free and in vitro assays, while superoxide dismutase-1 remains the only ALS-linked protein to demonstrate several prion-like properties in vivo. In this chapter, we provide an
introduction to ALS and review the recent literature linking several proteins implicated in the familial forms of the disease to properties of the prion protein.
The ALS network is on board with the idea:
The buildup of proteins in the brain and spinal cord is a hallmark of ALS. But how these proteins accumulate within the cells of the central nervous system in people with ALS remains a mystery.
Now, researchers from the University of Cambridge in England report that familial ALS type 1-associated superoxide dismutase 1 (SOD1) can spread from neuron to neuron. And once inside these neurons, these misfolded proteins can trigger the aggregation of the cells’ own copies of the enzyme.
These results suggest that ALS may be similar to prion diseases such as the brain disorder Creutzfeldt-Jakob disease. And at the same time, these findings suggest new therapeutic strategies to reduce the buildup of proteins in people with the disease.
In Theory, this now opens the path to research on treatments. Find a molecule that binds to the misfolded form and prevents the replication. Block the gene making the particular protein and hope you don’t need it. Etc.
It also confirms that injecting things shaped like that target is A Very Bad Idea…
NIH has an article too:
The prion-like nature of amyotrophic lateral sclerosis
L McAlary 1, J J Yerbury 1, N R Cashman 2
PMID: 32958236 DOI: 10.1016/bs.pmbts.2020.07.002
The misfolding, aggregation, and deposition of specific proteins is the key hallmark of most progressive neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). ALS is characterized by the rapid and progressive degenerations of motor neurons in the spinal cord and motor cortex, resulting in paralysis of those who suffer from it. Pathologically, there are three major aggregating proteins associated with ALS, including TAR DNA-binding protein of 43kDa (TDP-43), superoxide dismutase-1 (SOD1), and fused in sarcoma (FUS). While there are ALS-associated mutations found in each of these proteins, the most prevalent aggregation pathology is that of wild-type TDP-43 (97% of cases), with the remaining split between mutant forms of SOD1 (~2%) and FUS (~1%). Considering the progressive nature of ALS and its association with the aggregation of specific proteins, a growing notion is that the spread of pathology and symptoms can be explained by a prion-like mechanism. Prion diseases are a group of highly infectious neurodegenerative disorders caused by the misfolding, aggregation, and spread of a transmissible conformer of prion protein (PrP). Pathogenic PrP is capable of converting healthy PrP into a toxic form through template-directed misfolding. Application of this finding to other neurodegenerative disorders, and in particular ALS, has revolutionized our understanding of cause and progression of these disorders. In this chapter, we first provide a background on ALS pathology and genetic origin. We then detail and discuss the evidence supporting a prion-like propagation of protein misfolding and aggregation in ALS with a particular focus on SOD1 and TDP-43 as these are the most well-established models in the field.
Similar results for Alzheimer’s
Alzheimer’s Disease is a ‘Double-Prion Disorder,’ Study Shows
Self-Propagating Amyloid and Tau Prions found in Post-Mortem Brain Samples, With Highest Levels in Patients Who Died Young
By Nicholas Weiler
This is the caption for a fascinating photo:
The normal form of Aß has been tagged with a yellow marker in these cells, making healthy cells a uniform pale yellow (left). Contact with prion forms of Aß — for example in extracts from human brain tissue — forces these yellow proteins into the sticky prion form as well, leading to the formation of bright yellow clumps (right). Credit: Prusiner lab / UCSF Institute for Neurodegenerative Diseases.
Then back to the article body:
Two proteins central to the pathology of Alzheimer’s disease act as prions — misshapen proteins that spread through tissue like an infection by forcing normal proteins to adopt the same misfolded shape — according to new UC San Francisco research.
Using novel laboratory tests, the researchers were able to detect and measure specific, self-propagating prion forms of the proteins amyloid beta (Aß) and tau in postmortem brain tissue of 75 Alzheimer’s patients. In a striking finding, higher levels of these prions in human brain samples were strongly associated with early-onset forms of the disease and younger age at death.
Alzheimer’s disease is currently defined based on the presence of toxic protein aggregations in the brain known as amyloid plaques and tau tangles, accompanied by cognitive decline and dementia. But attempts to treat the disease by clearing out these inert proteins have been unsuccessful. The new evidence that active Aß and tau prions could be driving the disease – published May 1, 2019 in Science Translational Medicine — could lead researchers to explore new therapies that focus on prions directly.
“I believe this shows beyond a shadow of a doubt that amyloid beta and tau are both prions, and that Alzheimer’s disease is a double-prion disorder in which these two rogue proteins together destroy the brain,” said Stanley Prusiner, MD, the study’s senior author and director of the UCSF Institute for Neurodegenerative Diseases, part of the UCSF Weill Institute for Neurosciences. “The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease. We need a sea change in Alzheimer’s disease research, and that is what this paper does. This paper might catalyze a major change in AD research.”
At that point I ended the search for validation / confirmation.
It is clear that the specific claims about known prion diseases are accurate. It is clear that the spike protein and RNA vaccine have regions similar to prion mis-folding locations. There’s anecdotal evidence for some folks (limited in number) having “side effects” similar to the cited prion diseases.
I think that (barely) justifies the concern and saying “maybe, could be, possibly, risk, think about it…”
But is it TRUTH? Will we have Consequences? Is it an “and” or an “or”?
At this point nobody knows. But IMHO it is well worth watching and looking and testing and doing all that long term stuff that was skipped.
Me? I’ve had 3 occasions now of an “early onset sniffles & don’t feel right” that resolved the very next day with ONE application of Ivermectin Drench. (I’d rather get the proper deal from my M.D., but with The W.H.O., C.D.C, and N.I.H. all now Political Officer Driven, my M.D. is getting bad “advice” so I’m on my own now.) 10 ml, or the dose for a 200 lb / 100 kg sheep. For those of us who are not sheep… 1 x week or “one and done” in my case as by day 3 there’s nothing left to treat.
Were these Chinese Wuhan Covid onset? Or The Flu? Or The Common Cold? Or maybe even just allergies? No way to know, other than that allergies “feel different” to me and do not go away the next day (seasonal plants).
But even if just A Cold or The Flu, I’m happy with the result. Very happy. Guinea Pig One reporting ;-) but not going to be guinea pig for the two step experimental RNA “whack a gene” therapy…
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