The U.S. Food and Drug Administration has granted fast-tracking designation to UB-311, an Alzheimer’s vaccine manufactured by biotech company Vaxxinity.first This vaccine is a beta amyloid immunotherapy vaccine reported to treat Alzheimer’s disease by targeting synthetic beta amyloid in the brain.2
In addition to the potential problems that can arise when a vaccine is rushed to market, vaccines can be problematic in the first place because amyloid beta can be a symptom of Alzheimer’s disease – not the cause. – and may even have a protective role in the disease. process.3
Fast-tracking a vaccine that targets a single element of Alzheimer’s disease that isn’t the underlying cause would turn out to be a major disaster.
Alzheimer’s vaccine fast-tracked on market
UB-311 is being touted to induce “a robust and durable anti-amyloid beta antibody response in patients,” according to Vaxxinity.4 Long-term extended trials of Phase 1, Phase 2a and Phase 2a have been completed, with the company saying that the vaccine was “well tolerated in patients with mild to moderate AD over three years of dosing repeat, with a safety profile comparable to placebo and with no cases of amyloid-edema-associated imaging abnormalities (“ARIA-E”) in the primary study. ”5
ARIA-E, a marker of fluid retention and microbleeds in the brain, occurs in about one-third of people taking the Alzheimer’s drug aducanumab (brand name Aduhelm).6 Similar to UB-311, Aduhelm is marketed under the FDA’s expedited approval route, although clinical benefit is uncertain.7 The action sparked protests on the FDA’s advisory board, and three members subsequently resigned.8
As a beta amyloid-directed antibody drug, Aduhelm also works by targeting amyloid beta in the brains of people with Alzheimer’s disease, but the findings of ARIA-E in many people taking the drug are alarming. Adam Brickman of Columbia University, New York City, thinks the drug has the potential to make cognitive decline worse instead of better. “It is difficult to take a positive view of neuroimaging abnormalities,” he writes. “… [W]I simply don’t know the long-term consequences.”9
While Vaxxinity touts none of its subjects as successful cases of ARIA-E, the same is true about vaccines in that no one knows the long-term consequences. Vaxxinity has planned to test Phase 2b by the end of 2022.ten It should be noted that drug development for Alzheimer’s disease has so far been a flop, with at least 300 failed trials to date.11
One study, a collaboration between Washington University in St. Louis, the pharmaceutical companies Eli Lilly and Roche, the National Institutes of Health and others, had 194 participants, of whom 52 took Roche’s gantenerumab and 52 took Eli Lilly’s solanezumab.twelfth
The drugs were intended to remove amyloid beta (Aβ) from the brain, but they failed to achieve the main outcome of the study, which was slowing cognitive decline, as measured by tests of thinking and intelligence. miss.
In fact, while the drugs targeted amyloid beta, they did not affect cognitive measures, with the researchers writing, “Both drugs engaged in their Aβ targeting but both did not demonstrate beneficial effects on cognitive measures compared with controls.”13
Is Amyloid Beta the Problem?
Even if the drug reduces beta amyloid plaques in Alzheimer’s patients, what this means for cognitive decline remains to be seen. While Alzheimer’s disease is characterized by the accumulation of beta-amyloid plaques and neurofibrillary tangles in the brain, there is controversy about their role in the development of the disease.
As researchers from the Tokyo Metropolitan Institute of Health Sciences, the department of dementia and higher brain function, wrote in the journal Frontiers in Neuroscience:14
“The so-called amyloid hypothesis, that accumulation and deposition of oligomeric amyloid β (Aβ) or fibrillar peptides is the primary cause of Alzheimer’s disease (AD), has been a key concept in AD research for more than 20 years. five. However, every attempt to develop drugs that target Aβ for the treatment of AD has failed.”
In 2009, researchers drew attention to the false premise of simplifying Alzheimer’s disease to a protein precursor molecule amyloid-β (AβPP), “implying that the molecule encapsulates AD completely to the extent the disease itself is almost of secondary importance.” They note that this ignores the “complexity of chronic diseases in general” and adds:15
“A lot of attention has been focused on amyloid-β as the primary pathogenic mechanism with the ultimate goal of using amyloid-β-lowering therapies as a treatment. Unfortunately, almost a quarter of a century later, no concrete progress has been made, while spectacular failure tends to be the most compelling.
It has long been argued, as has been well documented, that protein accumulation is simply downstream and often the terminal manifestations of disease.
Their overall poor correlation with the degree of dementia, and their presence in cognitively intact condition is evidence that is often overlooked as a baffling fact. Therefore, the present study examining amyloid oligomers will add rich details about the nature, an agent that reduces distraction from upstream pleural inflammatory processes such as oxidative stress, dysfunction cell cycle function and inflammation.
It’s now too long for neuroscientists to get away from the trap of persevering with ‘protein pathology’ and realize that continuing to target end-stage lesions in the face of repeated failure repetition, or worse, a failed proposition. “
Amyloid Beta May Be Protected
There is even research that suggests that advanced protein combinations, such as those seen in Alzheimer’s disease, may provide protective functions, perhaps protecting cells from toxic mediators.16 Writing in the Annals of the New York Academy of Sciences, the researchers suggest that amyloid beta is a response to neuronal stress, which functions as an adaptive defense against disease.17
They argue that amyloid beta accumulates relatively late in the development of Alzheimer’s disease, and although it has been found to be toxic in cell culture models, this may not be the case in humans. Instead of the popular view that mutations lead to increased amyloid beta and lead to Alzheimer’s disease, the team proposed that mutations lead to Alzheimer’s disease, which in turn triggers increased beta amyloid:18
“Mutations that lead to cellular stress, in turn, lead to increased amyloid-β… in AD, cellular stress precedes increased amyloid-β… Proteins, such as amyloid-β, are made during conditioning Oxidative conditions and activity to reduce oxidative damage are generally considered antioxidants and in this respect, we have recently demonstrated that amyloid-β is a real antioxidant that can act as an antioxidant. Acts as a potent superoxide dismutase. ”
They suggest that this would explain why the brains of most elderly people contain amyloid-β, often in similar amounts as in patients with Alzheimer’s disease (AD). They note:19
“While such production and deposition of amyloid-β appears to successfully suppress age-related redox imbalances during normal aging, in AD, where oxidative stress is present, In deep and chronic reduction, the presence of amyloid-β, even at high levels, proves insufficient. ”
The link between Alzheimer’s disease and your gut
If the pathogenesis of Alzheimer’s disease cannot be entirely blamed on amyloid beta, what is the cause? It is likely to be caused by many factors, including an imbalance in the gut microbiome. Research shows, for example, that the bacteria in your gut can affect brain activity and may even promote neurodegeneration.20
In a study of 89 people, high blood levels of lipopolysaccharides (LPS) and short-chain fatty acids (SCFAs) acetate and valerate were associated with large amyloid deposition in the brain.21 LPS and SCFAs are markers of inflammation and proteins produced by gut bacteria.
High levels of butyrate – a SCFA produced when gut bacteria ferment fiber – was associated with less amyloid. The study represents a continuation of the team’s earlier work, which found that the gut microbiota in people with Alzheimer’s disease is different from that in those without the disease; In people with Alzheimer’s disease, microbial diversity is reduced, with certain bacteria being overrepresented and others reduced.22
Moira Marizzoni, study author of the Fatebenefratelli Center in Brescia, Italy, explains: “Our results are indisputable: several microbial products of the gut microbiome are correlated with the amount of the gut microbiome. amyloid plaques in the brain.23
Still other research suggests that the gut microbiome may contribute to Alzheimer’s risk through multiple pathways, including by influencing aging, diabetes, sleep, and rhythm biological.24
The researchers also hypothesized that decades of factors such as diet, stress, aging, and genetics combine to disrupt intestinal permeability and blood-brain barrier integrity. allows entry of inflammatory agents and pathogens and induces an inflammatory response. activating neuroinflammatory responses in the brain.25
There’s more to Alzheimer’s than Amyloid Beta
UB-311 – the rapid Alzheimer’s vaccine – will not address many of the complicating factors that lead to the development of Alzheimer’s disease and potentially unwanted adverse consequences. For example, dietary factors are being ignored altogether by focusing on vaccines that target beta amyloid.
What you eat affects not only your gut health, but also cholesterol, and cholesterol also plays an important role in memory formation and is essential for healthy nerve function. As noted by senior research scientist Stephanie Seneff, PhD, not enough fat and cholesterol in your brain plays an important role in the course of Alzheimer’s disease, detailed in her 2009 paper “APOE-4: The Clue to Why Low Fat Fat Diet and Statins May Cause Alzheimer’s Disease.”26
Time-restricted eating is another important strategy, as is reducing the amount of polyunsaturated fatty acids, also known as PUFAs, found in vegetable oils, cooking oils, nut oils, trans fats, and vegetable oils. . For a more targeted approach, organic options are available.
For example, animal and laboratory studies demonstrate that the spice saffron has neuroprotective effects. Data also suggest it is as effective as the drug memantine for treating moderate to severe Alzheimer’s disease.27 One of the most comprehensive assessments of Alzheimer’s risk is Dr Dale Bredesen’s ReCODE protocol, which assesses 150 factors, including biochemistry, genetics, and historical imaging, known to contribute to Alzheimer.
In her book, “The End of Alzheimer’s: A First Program to Prevent and Reverse Cognitive Decline,”28 which describes the complete procedure, you’ll also find a list of recommended screening tests and recommended ranges for each, along with some of Bredesen’s treatment recommendations.
Overall, nurturing your brain health is best done with a well-rounded healthy lifestyle. By taking advantage of 36 healthy lifestyle parameters, Bredesen was able to reverse Alzheimer’s disease in 9 out of 10 patients.
This includes the use of exercise, a ketogenic diet, optimizing vitamin D and other hormones, promoting sleep, meditation, detoxing and eliminating gluten and processed foods. For more details, you can download Bredesen’s full-text document online, which details the entire program.29
