An experimental Alzheimer’s vaccination appears to eliminate aberrant tau protein from the brain in a safe manner, but it is unclear if the injection will be able to save brain function.
The Alzheimer’s Vaccine Trial Delivers Both Positive And Negative Information
The vaccination produced high levels of antibodies to target and destroy free-floating tau proteins before they could form “tau tangles” that choke neurons and degrade brain function in Phase 2 clinical study. Tau tangles, along with plaques generated by the protein amyloid-beta, are one of the primary symptoms of Alzheimer’s disease.
While amyloid influences the rate of Alzheimer’s progression, there is strong evidence that tau pathology is linked to the disease’s underlying cause, according to lead researcher Dr. Novak, who is a senior clinical research scientist at AXON Neuroscience, the Slovakian pharmaceutical company developing the vaccine. Recent tau PET investigations show that brain shrinkage and cognitive decline closely mirror the buildup of pathogenic tau protein.
The vaccine was also found to be safe after a two-year experiment in which eleven doses were provided to people with moderate dementia who were chosen at random. People who got the AADvac1 vaccination had almost the same amount of side effects and adverse events as those who got a placebo.
The study, however, did not yield any substantial gains when it came to thinking, reasoning, and memory tests completed across the entire patient group – probably due to a small number of persons with clinically confirmed Alzheimer’s disease participating in the experiment.
During the clinical trial data analysis, the researchers discovered that around one-third of the individuals had low amounts of aberrant tau protein, making them unsuitable for testing the benefits of a medication that halts the advancement of tau pathology.
Novak stated that the study team did see modest improvement in routine brain function tests administered to a smaller sample of trial participants who had been diagnosed with Alzheimer’s.
In two distinct clinical and functional assessments, the vaccination delayed brain degeneration by roughly 30% in that group, according to Novak.
The findings precisely fit with the tau theory; simply put, if the patient is tau biomarker positive, tau pathology is to blame for his/her cognitive loss, and stopping tau pathology should slow or stop progression, according to Novak. If the patient tests negative for tau pathology indicators, the patient’s impairment is most likely attributable to other diseases, thus treating tau pathology in this patient is pointless.
According to Novak, AXON is preparing a follow-up experiment with a more defined sample of Alzheimer’s patients suffering from both amyloid plaques and tau tangles.
If the study findings are favorable, the business may seek to the US Food and Medicine Administration for the same fast approval process that was recently utilized to bring the controversial Alzheimer’s drug aducanumab to market, according to Novak.
In the present study, 196 individuals were randomly assigned to receive either the vaccination or a placebo.
According to Novak, nearly all patients who received the vaccination generated antibodies targeted to prevent the spread of aberrant tau proteins while leaving healthy tau proteins alone.
The immunization considerably decreased the buildup of the neurofilament light chain in the blood by 58 percent. According to Novak, this is a crucial diagnostic of neurodegenerative illnesses because injured nerve cells produce the chemical, which then seeps into the bloodstream.
According to the findings, patients who received the vaccination saw a decrease in cerebrospinal fluid indicators of aberrant tau.
Despite the trial’s relatively mixed findings, there is still potential for this strategy to treating Alzheimer’s disease, according to Rebecca Edelmayer, senior director of scientific engagement at the Alzheimer’s Association.
The vaccine approach is promising because using the body’s immune system to fight Alzheimer’s would avoid one of the challenges in developing a drug to treat the disease, namely the difficulty in designing medications that can easily enter the brain and attack a specific target, according to Edelmayer.