2nd Smartest Guy in the World

The following article was previously published on October 28th, 2023, but a few critical points must be explicitly reiterated about this Dementia & Alzheimer’s Disease Cure Protocol:

• Both Ivermectin and Fenbendazole must be taken with high fat meals to improve bioavailability
• Fenbendazole as per research studies is significantly more bioavailable when taken with a multivitamin or nutraceutical
• Fenbendazole is vastly superior to Mebendazole

Building on this protocol, in a recent research study titled, Hydroxychloroquine lowers dementia risk in humans, improves molecular signs of Alzheimer’s in mouse and cell models, the authors stated the following:

Taking hydroxychloroquine (HCQ) is linked to lower rates of Alzheimer’s disease and related dementias in people with rheumatoid arthritis, according to an international team of researchers led by NIA scientists. The study, published in Molecular Psychiatry, also included mouse and cell models to show that HCQ can improve early molecular signs of Alzheimer’s by reducing inflammation and enhancing the clearance of abnormal buildup of proteins that form amyloid plaques and neurofibrillary tangles. Because HCQ is already FDA-approved for other health conditions, these new study results could lay a strong foundation for clinical trials to test HCQ in older adults who are at high risk of developing dementia.

The authors concluded:

We recently nominated cytokine signaling through the Janus-kinase-signal transducer and activator of transcription (JAK/STAT) pathway as a potential AD drug target. As hydroxychloroquine (HCQ) has recently been shown to inactivate STAT3, we hypothesized that it may impact AD pathogenesis and risk. Among 109,124 rheumatoid arthritis patients from routine clinical care, HCQ initiation was associated with a lower risk of incident AD compared to methotrexate initiation across 4 alternative analyses schemes addressing specific types of biases including informative censoring, reverse causality, and outcome misclassification (hazard ratio [95% confidence interval] of 0.92 [0.83-1.00], 0.87 [0.81-0.93], 0.84 [0.76-0.93], and 0.87 [0.75-1.01]). We additionally show that HCQ exerts dose-dependent effects on late long-term potentiation (LTP) and rescues impaired hippocampal synaptic plasticity prior to significant accumulation of amyloid plaques and neurodegeneration in APP/PS1 mice. Additionally, HCQ treatment enhances microglial clearance of Aβ_1-42, lowers neuroinflammation, and reduces tau phosphorylation in cell culture-based phenotypic assays. Finally, we show that HCQ inactivates STAT3 in microglia, neurons, and astrocytes suggesting a plausible mechanism associated with its observed effects on AD pathogenesis. HCQ, a relatively safe and inexpensive drug in current use may be a promising disease-modifying AD treatment. This hypothesis merits testing through adequately powered clinical trials in at-risk individuals during preclinical stages of disease progression.

In a Nature article titled, Hydroxychloroquine lowers Alzheimer’s disease and related dementias risk and rescues molecular phenotypes related to Alzheimer’s disease, the authors showed an infographic for their study:

The Nature article concluded:

In summary, we have established that the commonly used RA drug, HCQ lowers AD risk in older individuals, and targets multiple pathogenic mechanisms in AD including synaptic dysfunction, neuroinflammation, Aβ clearance, and tau phosphorylation. Our results provide compelling evidence that this safe and inexpensive drug may be a promising disease-modifying treatment for AD. Confirmation of our findings in adequately powered clinical trials in at-risk individuals during preclinical stages of disease progression should be initiated in a timely manner.

The authors of the Nature study wrote a followup article titled, Hydroxychloroquine and Alzheimer’s disease, making some important clarifications:

Our paper, recently published in Molecular Psychiatry, suggests that hydroxychloroquine (HCQ), a relatively safe and inexpensive drug in current use, may be a promising disease-modifying Alzheimer’s disease (AD) treatment. The recent controversy around hydroxychloroquine’s use as a treatment for COVID-19 notwithstanding, the drug’s storied past and almost four centuries old history as a therapy for multiple diseases is a fascinating backdrop to our research.

Because Hydroxychloroquine stopped the gain-of-function (GOF) PSYOP-19 virus dead in its tracks such that there could never have been an “emergency” use authorization (EUA) granted by the captured FDA for their DEATHVAX™, and because wide administration of Hydroxychloroquine would have had positive side effects such as the significant reduction of Alzheimer’s and dementia in the populace, as well as prevention of curing of cancers…

…the powers that be had no choice but to smear and destroy Hydroxychloroquine, all while Dr. Fauci’s captured cadre of researchers deliberately designed flawed in vitro studies fraudulently demonstrating that Hydroxychloroquine would not be effective against their GOF plandemic (adding HCQ to low pH petri dishes approximating blood acidosis [cytokine storm phase post viral infection] in which case no compound works other than steroids), except that HCQ was around 100% effective against viral infections in real-world settings.

The researchers ended their op-ed with the following:

In summary, there is an urgent need to develop safe, effective, and easily accessible treatments for AD, which is a global public health challenge. Our research suggests that HCQ, an inexpensive, relatively safe and FDA-approved immune modulating drug in common use may benefit patients in early stages of AD by impacting multiple molecular pathways involved in the disease. These findings merit timely confirmation in adequately powered human clinical trials.

Hydroxychloroquine is also a powerful anti-inflammatory compound that only may be a treatment for Alzheimer’s Disease (AD) and cancer, but also autoimmune diseases like systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), offering significant benefits in preventing flares, reducing organ damage, and improving survival rates.

Thus, the latest revised AD protocol:

Dementia & Alzheimer’s Disease Cure Protocol

• Fenbendazole 150mg every other day with dinner for 30 days, and repeat every 4 months
• Ivermectin 12mg every evening with dinner indefinitely
• Low dose lithium orotate 4.8mg capsule in the morning with breakfast and in the evening with dinner indefinitely
• Hydroxychloroquine 200mg every evening with dinner indefinitely (“HCQ-associated lowering of AD risk emerges after approximately 2 years of treatment”)
• ImmunX immune support 2 capsules in the morning with breakfast indefinitely (Quercetin is a critical ingredient in ImmunX, and as per research studies similar to Ivermectin it displayed capabilities against tauopathy by inhibiting the hyperphosphorylation of the tau protein, thus its anti-prion activity helps to reverse Alzheimer’s Disease)
• Removal of sugars and carbohydrates, and replacing table sugar with a zero glycemic index, zero calorie, keto friendly rare sugar like AlluX
• Creatine Monohydrate 4 x 500mg capsules every evening with dinner indefinitely
• Methyl B-12 1 x 1,000mcg daily on empty stomach (water-soluble vitamins are better absorbed without food interference [given that AD’s patients have been shown to have severe vitamin B-12 decencies])
• A high fat diet, with daily ingestion of organic pasture eggs, and other quality fats (brain food that also greatly increases Ivermectin and Fenbendazole bioavailability)

Which brings us to the previously published article on the fungal infection thesis causing AD:

Some researchers have suggested that neurodegenerative diseases like Alzheimer’s, Parkinson’s, and multiple sclerosis may have a microbial origin; thus, inexpensive repurposed drugs may be the cure.

A recent article by The Epoch Times posited that fungal infections may be the cause of neurodegenerative diseases.

A team of researchers at Baylor College of Medicine has discovered that when the brain is infected with a common fungus, it changes in ways similar to those seen in Alzheimer’s disease. The new research delves deeper into some of the molecular mechanisms behind that process.

The Study Findings

Using animal models, the research team discovered how the fungus, called Candida albicans (C. albicans), enters the brain, activates mechanisms for its clearance, and generates amyloid beta (Aβ)-like peptides—toxic protein fragments thought to be central to the development of Alzheimer’s disease.

The findings were published Oct. 10 in the journal Cell Reports.

Previous research has implicated fungi in the development of chronic neurodegenerative diseases like Alzheimer’s disease, but their mechanisms are not entirely understood.

We know that Candida thrives on sugars, so diets high in processed junk foods may very well be feeding the funguses that in turn destroy brains.

We also know that the inexpensive and repurposed drug Fenbendazole eradicates these funguses; for example, a research study entitled, The Anti-helminthic Compound Mebendazole Has Multiple Antifungal Effects against Cryptococcus neoformans stated the following:

Cryptococcus neoformans is the most lethal pathogen of the central nervous system. The gold standard treatment of cryptococcosis, a combination of amphotericin B with 5-fluorocytosine, involves broad toxicity, high costs, low efficacy, and limited worldwide availability. Although the need for new antifungals is clear, drug research and development (R&D) is costly and time-consuming. Thus, drug repurposing is an alternative to R&D and to the currently available tools for treating fungal diseases. Here we screened a collection of compounds approved for use in humans seeking for those with anti-cryptococcal activity. We found that benzimidazoles consist of a broad class of chemicals inhibiting C. neoformans growth. Mebendazole and fenbendazole were the most efficient antifungals showing in vitro fungicidal activity. Since previous studies showed that mebendazole reaches the brain in biologically active concentrations, this compound was selected for further studies. Mebendazole showed antifungal activity against phagocytized C. neoformans, affected cryptococcal biofilms profoundly and caused marked morphological alterations in C. neoformans, including reduction of capsular dimensions. Amphotericin B and mebendazole had additive anti-cryptococcal effects. Mebendazole was also active against the C. neoformans sibling species, C. gattii. To further characterize the effects of the drug a random C. gattii mutant library was screened and indicated that the antifungal activity of mebendazole requires previously unknown cryptococcal targets. Our results indicate that mebendazole is as a promising prototype for the future development of anti-cryptococcal drugs.

Thus, we may extrapolate that Fenbendazole, being a powerful antifungal, may quickly and permanently reverse these kinds of neurodegenerative diseases.

(Mebendazole is vastly inferior to Fenbendazole, and only exists because BigPharma awarded itself a bogus patent as a money grab while offering a relatively ineffectual substitute.)

And precisely because C. albicans has been shown to generate toxic protein fragments like amyloid beta (Aβ)-like peptides in the brain, Fenbendazole would be an especially strong candidate for potential therapeutic use in Alzheimer’s treatment.

Back to The Epoch Times article, which reinforces this notion of fungal-induced cognitive decline:

Humans and C. albicans have a complicated relationship, as most of the time, C. albicans is harmless and is simply a member of a healthy microbiota. However, it is one of the few fungal species that cause disease in humans and is responsible for infections that range from superficial infections of the mucosa and skin, like thrush, diaper rash, and vaginal yeast infections, to more serious infections like invasive candidiasis that can affect the blood, heart, brain, and bones.

Infections by C. albicans are particularly dangerous for those with compromised immune systems, like those with AIDS, or people undergoing immunosuppressive therapies for cancer and other conditions. This suppression of the body’s defenses is part of the reason why some people acquire C. albicans infections after taking antibiotics, as they decrease the beneficial bacteria in the gut, causing an imbalance and allowing C. albicans to thrive. C. Albicans can survive outside the body and have the ability to colonize every human organ and tissue. According to the Encyclopedia of Microbiology, it is the most common cause of systemic fungal infections.

Since so much of humanity is now suffering from (subclinical) VAIDS, infections by C. albicans will become far more prevalent, as will the associated cases of Modified mRNA “vaccine”-induced early onset dementia and Alzheimer’s.

In a January review published in Frontiers in Immunology, researchers examined the role of fungus in central nervous system autoimmune and neurodegenerative disorders. The review states that recently, increasing evidence has pointed to the role of peripheral fungus in triggering inflammation, immune response, and worsening of a range of non-infectious disorders of the central nervous system (CNS), including multiple sclerosis, Parkinson’s, and Alzheimer’s disease.

The review concluded that fungus can trigger inflammation via different mechanisms in the progression of CNS non-infectious diseases, suggesting that it is crucial for developing future therapeutic agents and strategies.

A 2015 study published in Scientific Reports states that several researchers have proposed the possibility that Alzheimer’s disease may have a microbial cause. The researchers found evidence that tissue from the central nervous system (which includes the brain and spinal cord) of patients with Alzheimer’s disease contains fungal cells. These fungal cells were found in different regions of the brain, including the external frontal cortex, cerebellar hemisphere, entorhinal cortex/hippocampus, and choroid plexus. These fungal materials were not present in the control individuals who did not have Alzheimer’s disease. The researchers identified several different species of fungus in their samples.

What is of particular note are the surges of both blood clots and immunocompromisation coinciding with the DEATHVAX™ rollout, and the consequent increases of fungal infection susceptibility contributing to ever more deadly outcomes:

Interestingly, the study authors noted that fungal infection was also found in the blood vessels, which could explain the vascular pathology that is often found in Alzheimer’s patients.

Once again, the confluence of “vaccine” adverse events is truly curious.

The findings provide intriguing evidence that these fungal infections are present in the central nervous systems of those with Alzheimer’s disease and not in healthy individuals who served as the controls.

Given that over time the slow kill bioweapon injections cause increasingly larger swaths of society to become unhealthy, unvaccinated healthy individuals will serve as the ultimate controls, especially for increasingly prevalent diseases such as dementia and Alzheimer’s.

Another Piece of the Puzzle

Dr. Corry and his colleagues have provided another piece to further understand the role fungus may play in the development of Alzheimer’s disease.

“This work potentially contributes an important new piece of the puzzle regarding the development of Alzheimer’s disease,” Corry said in a press release. “The current explanation for this condition is that it is mostly the result of the accumulation of toxic Aβ-like peptides in the brain that leads to neurodegeneration. The dominant thinking is that these peptides are produced endogenously [internally], our own brain proteases break down the amyloid precursor proteins generating the toxic Ab peptides.”

Due to their anti-prion activity, the other pieces of the therapeutic puzzle are Ivermectin and Quercetin (ImmunX has the perfect daily serving of Quercetin).

Ivermectin, another antiparasitic drug, was shown by Kawasaki et al. (2007) to have prevented the formation of the infectious form of the prion protein in prion-infected cells. Meanwhile, Quercetin, a flavonoid, extended the lifespan of prion-infected mice, highlighting its therapeutic potential against prion diseases.

Both compounds have also exhibited properties that modulate tauopathy, a characteristic of Alzheimer’s disease. Ivermectin inhibited tau hyperphosphorylation and even disaggregated tau fibrils. Quercetin, too, displayed capabilities against tauopathy by inhibiting the hyperphosphorylation of the tau protein.

The discovery of Fenbendazole, Ivermectin, Hydroxychloroquine, and Quercetin’s potential therapeutic properties underscores the importance of repurposing existing drugs in order to create highly accessible new treatment paradigms for neurodegenerative diseases.

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