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Can You "Catch" Alzheimer's Disease?

STORY AT-A-GLANCE This story is about the microbial theory of Alzheimer's disease.

Can You "Catch" Alzheimer's Disease?

Why am I writing about it? I am writing about it because it's like unraveling a detective plot. There is a disease that they say a lot of people have — and that is caused, they say, by amyloid deposits in the brain. But then it turns out that the currently widely accepted narrative about this disease is based on forged research . Then more research shows up suggesting that amyloid deposits might be a reaction, an immune response to something, even though nobody seems to know exactly to what. Then there are general debates about brain microbiome , an admission that our brain is not sterile, and also growing evidence that a number of microorganisms (including bacteria, fungi, and especially parasites that are more common that we westerners give

ourselves credit for ) can cause a significant infiammatory response in the brain — resulting in symptoms associated with Alzheimer's disease. To add to the complexity of the plot, it is probably logical to assume that the microbes — whichever microbes they are — would have a much harder time causing wreckage if our bodies and our environments weren't poisoned so devastatingly, so through and through. But environmental toxicity is a part of our lives, it is superimposed on us (and COVID "vaccines" didn't help). And because we are living in a world that unavoidably poisons us as we go about daily lives (hi, glyphosate, synthetic biology , geoengineering , aluminum, shedding, and EMFs!), I am writing this because it is practical to try and understand how those microbial interactions work in our current conditions and maybe acknowledge the fact that we don't live in an ideal world where it's easy to maintain the microbiome and the immunity of supergods. We are like trees in a poisoned desert, stretching our branches toward the sun no matter what, fighting for life no matter what, and we will be stronger if we look at all factors involved. (Yes yes, I am nodding at the famous debate about germ vs. terrain that — in its extreme form — seeks to strike down the concept of contagion as such, which to my senses is rather contrived since both germs and terrain exist — in fact they are rather intermixed — and they both play a role in this very complex world of ours.) On a side note, to illustrate my general point that our understanding of the world tends to evolve and that it's good to keep an open mind, the scientific community just recently discovered a whole new part of the brain ! Anyway, the biology and the etiology of AD is one part of the detective plot. But in parallel to the plot about the inner workings of our bodies, there is another detective story brewing underneath. That other plot is about financial and political factors that determine the timing of narrative "release." And today, as the story of the infection possibly causing AD is quietly brewing in the mainstream ( National Institute of Aging , Harvard , JAMA , Guardian , BBC , NPR , CBS , the New York Times ), there is talk about using vaccines to prevent pathogen-driven AD. There is even talk about fiu vaccines preventing AD! Case in point :

"Two studies presented Monday (July 27) at this year's virtual Alzheimer'sAssociation International Conference have demonstrated that fiu andpneumococcal vaccines are linked with a lower risk of Alzheimer's disease.In both studies, individuals who had received at least one vaccination — a fiushot in one study, and a pneumonia vaccine with or without a fiu shot in thesecond — were less likely to be diagnosed with Alzheimer's later in life. Whilethe studies are slightly different, their similar conclusions suggest that vaccinesmay play a broader role in strengthening a person's lifelong resistance to somediseases."

Also this. In meanwhile though, the increasing popularity of the "infectious" AD hypothesis didn't hold the FDA back from granting a fast-track designation to UB-311, an anti-A β antibodies-based "vaccine for Alzheimer's disease made by biotechnology company Vaxxinity," which they did in May 2022. Better safe than poor! As of January 2023, the company is seeking a partner for Phase 3 development, and has not registered nor begun a large trial of UB-31. On the infectious side, there is talk about shingles being to blame for AD — and we know about the new push for the shingles vaccine. If the narrative about that link gets favored, we can only imagine the pressures mounted to get everyone vaccinated against shingles in order to prevent AD and becoming a burden on your loved ones and the state, etc. (Or else MAID?) In a separate subplot, there is also ongoing research into vaccines against Toxoplasma gondii, the intracellular parasite that could be complicit in AD . The vaccines they've been working on may come in different forms , including a DNA vaccine and — for animals, currently — as a rather sour-sounding oral vaccine consisting of a genetically modified version of the parasite . (Unrelatedly, here's one for Lyme that could "come as soon as 2025." They are on a roll!) One could say, so what, there is always talk about vaccines against everything under the sun, they can talk! Yes, that's true, there is always talk about them since the "v-word" is a famous cash cow and a required talking point in the mainstream. However, in the light of the past three years and in the context of an objectively existing malaise (dementia, in this case) and an objectively prevalent but often misdiagnosed and misunderstood parasite (Toxoplasma g.), that direction of conversation alarms me quite a bit. And methinks that it's better for us to educate ourselves and start thinking it through now. It would also tremendously help if the doctors with honest minds decided to investigate it thoroughly with our actual health in mind, before the robo-eyed ones try to force a new "health countermeasure" on us that doesn't help and that we hadn't asked for. And that is why I think we should talk about it now. On my end, I would like to loudly proclaim a divorce of exploring how things work from anyone's push for "vaccines" — and it is easier to do that preemptively, before the syringe is prepared, and the conversation about infectious AD goes full mainstream.

What Is Alzheimer's Disease, Anyway?

Given the prevalence of Alzheimer's disease in elders and the amount of funding the topic receives, one would think that at the very least, we'd have a reliable definition of the disease and a solid way to diagnose. But not so fast, soldier, not so fast. Let's start with the basics. Per Science , "one of its biggest mysteries is also its most distinctive feature: the plaques and other protein deposits that German pathologist Alois Alzheimer first saw in 1906 in the brain of a deceased dementia patient. In 1984, A β [protein amyloid beta] was identified as the main component of the plaques. And in 1991, researchers traced family-linked Alzheimer's to mutations in the gene for a precursor protein from which amyloid derives. To many scientists, it seemed clear that A β buildup sets off a cascade of damage and dysfunction in neurons, causing dementia. Stopping amyloid deposits became the most plausible therapeutic strategy." And according to the NIH , "higher levels of beta-amyloid are consistent with the presence of amyloid plaques , a hallmark of Alzheimer's disease." Additionally, "most widely used CSF [cerebrospinal fiuid] biomarkers for Alzheimer's disease measure beta- amyloid 42 (the major component of amyloid plaques in the brain), tau , and phospho-tau (major components of tau tangles in the brain, which are another hallmark of Alzheimer's)." The societal handling of Alzheimer's is a microcosm refiecting the macrocosm of our culture and economics at large. And so, If I were to think this through like an intellectually honest five-year-old child, I would ask these questions: • When Alois Alzheimer, the German pathologist who gave the disease its name, discovered those plaques in the deceased patient's brain, could he or anyone else know that the plaques he had found were the cause of dementia and not a byproduct of something else that was going on, like an infiammatory presence of bacteria or parasites? • An extracurricular question? Why do the scientists of today like to assume that our bodies are broken machines — and not wise wonders who usually do things for a reason? Why? • Later, when the scientists claimed that they had found a reliable biomarker of Alzheimer's disease, did they gain a new insight into the causation of AD — or did they just make a conventional industry-wide agreement to use the AD diagnosis whenever the biomarker was found? (Incidentally, I know the answer to that question. It's the latter. I learned about it in 2019 at a legal conference about the ethics of AI (or something along those lines) and I remember how perplexed I was to learn from a doctor panelist that once the AD biomarker had been adopted as the primary way to diagnose the disease, some patients with the biomarker but without dementia would be diagnosed as AD, while other patients with dementia but without the biomarker would be left with a "mystery disease.") Little did I know how "interesting" the following year of 2020 would be in that sense! • And what if Alzheimer's disease is not really one disease but an umbrella term for a heap of conditions caused perhaps by infiammation in the brain, and what if — so shocking and novel, I know! — infiammation can be caused by multiple factors, and when the scientists make confident statements about the cause of Alzheimer's Disease, they are mostly poking their fingers into the sky and pufing cheeks to justify their grants — while having very little idea about what causes what?

Speaking of Pufing Cheeks, the Fraud

Daily Kos :

"Over the last two decades, Alzheimer's drugs have been notable mostly forhaving a 99% failure rate in human trials.It's not unusual for drugs that are effective in vitro and in animal models to turnout to be less than successful when used in humans, but Alzheimer's has arecord that makes the batting average in other areas look like Hall of Famematerial ... And now we have a good idea of why.Because it looks like the original paper that established the amyloid plaquemodel as the foundation of Alzheimer's research over the last 16 years mightnot just be wrong, but a deliberate fraud."

As a result, in late 2022, an "ultimate" trial of the amyloid hypothesis was launched.

Infectious Hypothesis: A One-Million-Dollar Challenge

In early 2018, Dr. Leslie Norins of Alzheimer's Germ Quest (their website is no longer live) announced a one-million-dollar challenge award for the scientist who would find the germ causing Alzheimer disease. The challenge lasted three years, and in February 2021, the press release said that "eight final honorees will divide $200,000 for meritorious entries in Alzheimer's Germ Quest's '$1 Million Challenge.' However, nobody provided persuasive-enough evidence that a particular infectious agent was the sole cause of Alzheimer's disease, so the grand prize of $1 million will not be awarded … Six microorganisms were nominated: herpes, toxoplasma, Borrelia, mycobacteria, H. pylori, and P. gingivalis."

Toxoplasma Gondii

  • gondii, averaging from 11-20% in the United States to 50% and higher in some
  • Western European countries
  • Alzheimer's disease and various other neurological disorders, as well as in heart
  • disease, pneumonia, recurrent headaches, even cancer; it is also known for causing
  • psychological changes in its hosts
  • asymptomatic, the impact of the parasite could be much more devastating than the
  • current mainstream medical convention presumes; it may also be cross-reacting with
  • the spike protein and possibly contributing to the mystery of "long COVID"
  • previously considered harmless in immunocompetent patients, are capable of
  • causing major health issues without converting to the cell-blasting form
  • blasting) form of the parasite but not the "bradyzoite" (tissue cyst) form

I wrote about this tricky parasite last year, and I think it calls for a good look in the context of its prevalence in the population and the glaring gap between the recent toxoplasma research and the outdated information that they seem to teach doctors in medical school. In the AD research world, toxoplasma is getting less of a spotlight than it deserves — but in the toxoplasma research world, its connection to Alzheimer's has come up multiple times. Here is the summary of what my earlier article said: • At least one third of all people on Earth are infected with the parasite Toxoplasma gondii, averaging from 11-20% in the United States to 50% and higher in some Western European countries • The parasite has been implicated in ocular issues, schizophrenia, epilepsy, Alzheimer's disease and various other neurological disorders, as well as in heart disease, pneumonia, recurrent headaches, even cancer; it is also known for causing psychological changes in its hosts • While the oficial word is that most toxoplasma infections are harmless and asymptomatic, the impact of the parasite could be much more devastating than the current mainstream medical convention presumes; it may also be cross-reacting with the spike protein and possibly contributing to the mystery of "long COVID" • According to recent research and clinical evidence, toxoplasma tissue cysts, previously considered harmless in immunocompetent patients, are capable of causing major health issues without converting to the cell-blasting form • Commonly used antibody tests can only detect antibodies for the "tachyzoite" (cell- blasting) form of the parasite but not the "bradyzoite" (tissue cyst) form

The State of the Alzheimer's 'Infectious' Hypothesis

According to a 2020 paper tilted, "Infectious hypothesis of Alzheimer disease":

"The infectious hypothesis proposes that a pathogen (virus, bacteria, prion,etc.) is the root cause of AD [2]. The hypothesis is supported by evidence thatsome pathogens, such as herpesviruses and certain bacterial species, arefound more commonly in AD patients. There is some variation within theinfectious hypothesis field as to how an infectious pathogen explains thepathological hallmarks of AD.Direct infection and eventual death of central nervous system (CNS) cells bypathogens could explain the cognitive deficits and heightened infiammationfound in AD [3].The relationship between infiammation and the AD hallmarks has long beenrecognized, with infiammation hypothesized to cause tissue damage, leading toprotein aggregates such as Aβ plaques and tangles, which in turn can lead tomore infiammation [4].""This cascade could be initiated by a number of endogenous and externalfactors, including microbial pathogens. Alternatively, Aβ and tau may be theproducts of normal responses to infection, intended to sequester threats to theCNS [5].Accumulation of Aβ and tau could then occur when the generation of theaggregates outpaces clearance by the microglia in the brain, a process broughtabout by the natural process of aging [5] …The aggregates themselves have shown to trigger neuroinfiammation as well[6]. Recent findings have highlighted a number of pathogens as potential driversof AD, but the family of pathogens most investigated is the herpesviruses [7]."

And here is a 2021 BBC story titled, "Alzheimer's: The heretical and hopeful role of infection":

"To date, the most compelling evidence for the infection hypothesis comes froma large study in Taiwan, published in 2018, which looked at the progress of8,362 people carrying a herpes simplex virus. Crucially, some of theparticipants were given antiviral drugs to treat the infection.As the infection hypothesis predicted, this reduced the risk of dementia. Overall,those taking a long course of medication were around 90% less likely todevelop dementia over the 10-year study period than the participants who hadnot received any treatment for their infection.Scientists studying the infection hypothesis have also started making someheadway in explaining the physiological mechanisms. Their explanation centreson the surprising discovery that amyloid beta can act as a kind of microbicidethat fights pathogens in the brain.Studies by Fulop and others, for instance, show that the protein can bind to thesurface of the herpes simplex virus. This seems to entrap the pathogen with aweb of tiny fibres and prevents it from attaching to cells. In the short term, thiscould be highly advantageous, preventing the infection from spiralling out ofcontrol so that it poses an immediate danger to someone's life.But if the pathogen is repeatedly reactivated during times of stress, the amyloidbeta could accumulate in the toxic plaques, harming the cells it is meant to beprotecting.As interest in the infection hypothesis has grown, scientists have started toinvestigate whether any other pathogens may trigger a similar response — withsome intriguing conclusions. A 2017 study suggested that the virus behindshingles and chickenpox can moderately increase the risk of Alzheimer'sdisease.There is also evidence that Porphyromonas gingivalis, the bacterium behindgum disease, can trigger the accumulation of amyloid beta, which may explainwhy poor dental health predicts people's cognitive decline in old age. Certainfungi may even penetrate the brain and trigger neurodegeneration. If thecausal role of these microbes is confirmed, then each finding could inspire newtreatments for the disease."

And the screenprint below is from a 2021 presentation by the National Institute of Aging under NIH.

What About Infectivity?

The funny thing is that billions of dollars in funding later, the honest answer is that nobody knows. That's the humbling part. The earlier mainstream conviction is that it is obviously not infectious because it's caused by amyloid plaques. With that hypothesis possibly on its way out, we are back to the drawing board. When Dr. Leslie Norins announced his one-million-dollar challenge award, he mentioned a few studies that suggested an infectious route. A 2010 study published in the Journal of Neurosurgery showed that neurosurgeons die from Alzheimer's at a nearly 2 1/2 times higher rate than the general population. Another 2010 study, published in The Journal of the American Geriatric Society, found that people whose spouses have dementia are at a 1.6 times greater risk for the condition themselves. And if Toxoplasma gondii has anything to do with it, then up until a certain point, there were papers published showing possible horizontal transmission ( here and here ) — but then they stopped. Was it because it was concluded that horizontal transmission did not exist? Was it because there was nothing lucrative to sell, while the symptoms could be blamed on something else? I don't know. But in any case, the most insane idea in my book would be to not hug our loved ones, Alzheimer's or not.

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