Alzheimer’s like brain damage caused by the COVID vaccine may be more prevalent than brain damage caused by naturally acquired virus, according to a a senior research scientist at the Massachusetts Institute of Technology.
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It is only a sniffle for some. COVID-19, on the other hand, can have a significant impact on some people. In either case, some individuals who are exposed to COVID-19 will experience long-term consequences. This is referred to as “long COVID,” and those that suffer from it are known as “long haulers.” Long COVID is likely already familiar to you, and you may have been impacted or know someone who has been. What is less generally understood, however, is that lengthy COVID is associated with a high rate of neurological problems.
After infection with the SARS-CoV-2 virus, brain inflammation, stroke, chronic headache, disrupted consciousness, cognitive impairment, and “brain fog” (an all-encompassing term for a syndrome that typically appears as slow thinking, memory lapses, and difficulties concentrating) can all occur.
Hyposmia and hypogeusia—commonly referred to as loss of smell and taste by non-scientists—are hypothesized to be caused by abnormalities in nerve system activity.
However, while physicians and patients have reported a variety of brain problems following infection, scientists are still learning more about how SARS-CoV-2 infections can affect brain function.
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That may be changing.
A study released in Alzheimer’s & Dementia (read below) on February 3 gives insight on a possible physiological basis behind the neurological issues COVID-19 survivors face.
While having a better understanding of what is going on is encouraging, there is also some bad news.
“Alzheimer’s-Like Signaling in Brains of COVID-19 Patients,” a recent study, contains some alarming discoveries.
Attacking ACE2 Receptors
The research, directed by Andrew R. Marks, a cardiologist and chair of the Department of Physiology and Cellular Biophysics at Columbia University’s Vagelos College of Physicians and Surgeons in Manhattan, examined brain tissue from ten individuals who died of COVID-19.
Marks’ team examined the brains of four women, aged 38 to 80, and six males, ages 57 to 84, after they died.
The spike protein of SARS-CoV-2 is already recognized to attach to ACE2 receptors throughout the body, particularly in the heart, lungs, kidneys, and epithelial cells that line blood vessels.
Scientists furthermore believe that this infiltration of heart and lung cells via these ACE2 receptors is probably the cause of the multi-system failure that might result in mortality from COVID-19.
Scientists said in a 2021 post published on The Conversation that since the virus has infected the receptors, the functioning of the enzyme linked with the receptors (angiotensin-converting enzyme) has been lowered.
When patients are sick, the damage to the lungs and heart is frequently the first thing on doctors’ minds. However, it turns out that ACE2 receptors can also be found in the brain.
This is pretty technical unless you are a neurologist. Regardless, stick with me. Reduced ACE2 activity is linked to increased transforming growth factor-beta (“TGF-beta”) activity. High levels of TGF-beta in the brain are linked to abnormalities in the “tau” proteins that maintain nerve cells, owing to a process known as “hyperphosphorylation.”
The addition of phosphate to an organic molecule, in this case the tau protein, is a normal biological process named Phosphorylation.
The insertion of too many phosphate groups at too many locations is referred to as hyperphosphorylation.
Proteins with extra filaments can become tangled as a result of hyperphosphorylation. These tau filament “tangles” have been linked to Alzheimer’s disease.
Marks and his five Columbia University colleagues explored whether individuals who died from COVID-19 had tau protein abnormalities, which are linked to Alzheimer’s.
A considerable amount of recent research shows that tau abnormalities may be caused by calcium ions “leaking” from particular ion channels in the brain known as ryanodine receptors.
Ion channels allow ions to pass through cell membranes, including those of brain cells (neurons). In a nutshell, ions allow electrical charges to flow throughout the body, and this flow is vital to the proper functioning of all cells. It is, in some ways, the body’s communication system and one of the major mechanisms of brain function.
Healthy brain activity is dependent on ion channels, such as the ryanodine receptors stated earlier, working properly. There are problems when these ion channels leak ions, just as there are hazards when an electrical cable is “leaking” power owing to a short. Calbindin, a protein that helps maintain these channels closed and prevents them from leaking, may be depleted as a result of oxidative stress. When calbindin levels are low, calcium leaks through channels that should be closed.
A buildup of calcium ions in the brain or elsewhere in the body can lead to a variety of health issues.
Marks’ team looked for signs of leakage in the brain tissue of the ten persons who died from COVID.
More precisely, they looked for indicators of TGF-beta activity in brain tissue. TGF-beta activity was observed to be elevated in both the cortex and the cerebellum. They also discovered signs of elevated oxidative stress.
Alzheimer’s patients have tau filament “tangles” exclusively in the cortexes of their brains, not in the cerebellum.
However, unlike Alzheimer’s, this Columbia University study found that COVID may also cause cerebellar dysfunction.
According to the University of Texas Health Science Center, the cerebellum is involved in balance, movement coordination, language, and posture.
According to other recent research, 74% of hospitalized COVID patients report coordination issues. If COVID is affecting both the cerebellum and the cortex, it may help to explain the coordination deficits that physicians have observed.
Amusingly, despite the small size of the study, all of the individuals who died had indications of brain pathology. The TGF-beta signature was discovered in all of the brains studied, including those of younger individuals who had shown no signs of dementia previous to contracting COVID-19.
Most individuals are aware that the existence of beta-amyloid plaques in the brain indicates Alzheimer’s disease. Despite the fact that decreased ACE2 activity is related with an increase in beta-amyloid plaques, the Columbia researchers found no alterations in the pathways that contribute to the development of amyloid beta in the brains of COVID patients (with the exception of one 84-year-old male who was previously suffering from dementia). This is one major distinction between COVID-19 pathology and Alzheimer’s or dementia pathology.
Treating Neurological Symptoms
Marks has a long history of interest in ryanodine ion channels, and his current COVID-related study could lead to financial rewards if other researchers confirm his findings. In 2011, a study team lead by Marks discovered that Rycals, a class of medicines, may be beneficial in treating heart failure and muscle diseases by stabilizing the same ryanodine ion channels implicated in COVID-19 infections.
One medicine in this class, ARM210, has been in clinical trials but has been designated as an orphan drug due to the rarity of the ailment it was designed to treat.
Marks informed ScienceDaily that his research points to a possible target for therapeutic approaches for COVID’s neurological symptoms.
“My greatest hope is that other laboratories will look into our findings, and if they are validated, generate interest in a clinical trial for long COVID,” he said.
Columbia University and Marks are both shareholders in ARMGO Pharma, Inc., a business that is researching medications that target ryanodine channels. According to a conflict of interest statement at the bottom of this study, they also own patents on Rycals. Steven Reiken, another research co-author, has been advising with ARMGO. While such conflicts of interest are very common in published scientific research and do not discredit the research, they are a significant element of the entire picture that should not be overlooked.
It is also not uncommon for a medicine developed for one reason to find fresh life addressing another. In some situations, these additional applications prove to be more vital than the drug’s original intended usage.
In their paper, the Columbia team wrote that “ex vivo treatment of COVID-19 patient brain samples with the Rycal drug ARM210 … fixed the channel leak.”
While this suggests a promising direction for future research, applying a medicine to brain cells in the lab is a considerable distance from administering it to actual individuals.
Vaccine-Linked Neurological Damage
While COVID has been associated to neurological disorders, the vaccine seems to be the same. Stephanie Seneff, a senior research scientist at the Massachusetts Institute of Technology and author of the book “Toxic Legacy,” is afraid that COVID-19 vaccinations may cause brain damage as well.
“Vaccines produce the spike protein, which is the part of the virus that binds to the ACE2 receptors,” said Seneff, who wasn’t involved in the Columbia research. “I suspect this means that the vaccine could also disable the receptors and cause the same neurological damage.”
According to Seneff, brain damage caused by the vaccine may be more prevalent than brain damage caused by naturally acquired virus. Vaccine-induced spike proteins “get into the brain more easily than the virus does,” she said. “The virus only gets into the brain when a person has a compromised immune system. But the vaccine is injected into the muscle, which means it bypasses natural barriers that would normally keep the virus out of the brain.”
Seneff and her colleague Dr. Greg Nigh, an oncologist based in Portland, Oregon, submitted a study in the peer-reviewed International Journal of Vaccine Theory, Practice, and Research in May 2021, stating their idea that mRNA vaccines may be as bad as the disease itself.
She has been reviewing reports of vaccination adverse events collected by the Centers for Disease Control and Prevention since then, she claims. Seneff discovered in this recent study that COVID vaccinations are responsible for 96 percent of all documented bad effects related to neurological disorders in the year 2021. Memory problems, movement problems, difficulties swallowing, and a loss of sense of smell are among the adverse neurological occurrences.
“All these things that are showing up in VAERS are striking,” Seneff said. “Overwhelmingly, the events that show neurological issues are following COVID-19 vaccines. I honestly don’t know why people aren’t absolutely shocked by these numbers. Compared to the other vaccines, these vaccines seem tremendously dangerous.”
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