The U.S. Food and Drug Administration granted fast-track designation to UB-311, a vaccine for Alzheimer’s disease made by biotechnology company
Aside from the potential problems that can arise when a vaccine is rushed to market, the vaccine may be problematic from the get-go because amyloid beta may be a symptom of Alzheimer’s, not the cause
Researchers have even suggested that amyloid beta is a response to neuronal stress, one that functions as a protective adaptation to the disease
Fast-tracking a vaccine that’s targeting an isolated element of Alzheimer’s disease that is not the underlying cause is destined to be a massive disaster
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The U.S. Food and Drug Administration granted fast track designation to UB-311, a vaccine for Alzheimer’s disease made by biotechnology company Vaxxinity.1 The shot is an anti-amyloid beta immunotherapeutic vaccine that reportedly treats Alzheimer’s disease by targeting aggregated amyloid beta in the brain.2
Aside from the potential problems that can arise when a vaccine is rushed to market, the vaccine may be problematic from the get-go because amyloid beta may be a symptom of Alzheimer’s — not the cause — and could even have a protective role in the disease process.3
Fast-tracking a vaccine that’s targeting an isolated element of Alzheimer’s disease that is not the underlying cause is destined to be a massive disaster.
Alzheimer’s Vaccine Being Fast-Tracked to Market
UB-311 is being touted for eliciting a “robust and durable anti-amyloid beta antibody responses in patients,” according to Vaxxinity.4 Phase 1, Phase 2a and Phase 2a long-term extension trials have already been completed, with the company stating that the vaccine was “well tolerated in mild-to-moderate AD patients over three years of repeat dosing, with a safety profile comparable to placebo and no cases of amyloid-related imaging abnormalities-edema (“ARIA-E”) in the main study.”5
ARIA-E, a marker of fluid retention and microhemorrhages 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 was brought to market under an accelerated approval pathway by the FDA, despite uncertainty about the clinical benefit.7 The action sparked protests within the FDA advisory panel, and three members subsequently resigned.8
As an amyloid beta-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 taking the drugs are alarming. Adam Brickman with Columbia University, New York City, suggested that the drug could potentially make cognitive decline worse instead of better. “It’s hard to put a positive spin on the neuroimaging abnormalities,” he wrote. “… [W]e simply do not know the long-term consequences.”9
While Vaxxinity is touting no cases of ARIA-E among its subjects as a success, the same holds true about the vaccine in that no one knows the long-term consequences. Vaxxinity has planned a Phase 2b trial for late 2022.10 It’s worth noting that drug development for Alzheimer’s has so far been a dismal failure, with at least 300 failed trials to date.11
One study, which was a collaboration between Washington University in St. Louis, drug companies Eli Lilly and Roche, the National Institutes of Health and others, involved 194 participants, of which 52 took Roche’s drug gantenerumab and 52 took Eli Lilly’s solanezumab.12
The drugs were intended to remove amyloid beta (Aβ) from the brain, but they failed to achieve the primary outcome of the study, which was slowed cognitive decline, as measured by tests on thinking and memory.
In fact, while the drugs did target amyloid beta, they had no effect on cognitive measures, with the researchers writing, “Both drugs engaged their Aβ targets but neither demonstrated a beneficial effect on cognitive measures compared to controls.”13
Is Amyloid Beta the Problem?
Even if drugs reduce amyloid beta plaques in Alzheimer’s patients, how this translates to affecting cognitive decline remains to be seen. While Alzheimer’s is characterized by an accumulation of beta-amyloid plaques and neurofibrillary tangles in the brain, there is controversy over their role in the development of the disease.
As researchers from the Tokyo Metropolitan Institute of Medical Science, department of dementia and higher brain function, wrote in Frontiers in Neuroscience:14
“The so-called amyloid hypothesis, that the accumulation and deposition of oligomeric or fibrillar amyloid β (Aβ) peptide is the primary cause of Alzheimer's disease (AD), has been the mainstream concept underlying AD research for over 20 years. However, all attempts to develop Aβ-targeting drugs to treat AD have ended in failure.”
In 2009, researchers brought attention to the misguided premise of oversimplifying Alzheimer’s disease down to the amyloid-β protein precursor (AβPP) molecule, “implying that this molecule encapsulates AD so completely that the disease itself is almost of secondary importance.” This, they noted, ignores “the complexity of chronic diseases in general” and added:15
“A great deal of attention has focused on amyloid-β as the major pathogenic mechanisms with the ultimate goal of using amyloid-β lowering therapies as an avenue of treatment.