Alzheimer's disease might be cured with a new method.

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A team of UK and German scientists has devised a promising new technique to possibly treat Alzheimer's disease—as well as vaccinating against it. Alzheimer's symptoms in mice models were decreased by antibody-based therapy and protein-based vaccination created by the researchers. The findings have been published in Molecular Psychiatry. Researchers from the University of Leicester, the University Medical Center Göttingen, and the LifeArc medical research foundation collaborated.

The antibody and vaccination both target a distinct soluble version of the protein, which is considered particularly hazardous, rather than the amyloid-beta protein seen in brain plaques, which is frequently linked with Alzheimer's disease.

To form fibrils and plaques, and amyloid-beta protein naturally occurs in solution in the form of highly flexible, string-like molecules that may come together. Researchers believe that Alzheimer's disease is caused by the shortening of these string-like molecules, known as "truncated" molecules, in patients.

"In clinical studies, none of the prospective medicines that remove amyloid plaques in the brain has shown significant efficacy in terms of lowering Alzheimer's symptoms," stated Professor Thomas Bayer of the University Medical Center Göttingen. "Some people may have harmful impacts as a result. Because of this, we came up with a new strategy. An antibody can neutralize Amyloid-beta shortened versions in mice, but normal protein or plaques cannot be bound by it."

Dr. Preeti Bakrania and her colleagues at LifeArc altered this antibody such that it would not be recognized as foreign by the human immune system and would be accepted. This 'humanized' antibody, named TAP01_04, was shown to be binding to the shortened form of amyloid-beta by the Leicester research team. In a hairpin-shaped structure, they discovered the amyloid-beta protein.

According to Professor Mark Carr of Leicester's Institute of Structural and Chemical Biology, an amyloid-beta structure that has never been seen before has been discovered. It was possible to modify this area of the protein to maintain the hairpin shape and bind to the antibody in the same manner because of the discovery of a clear structure. Amyloid-beta might be utilized as a vaccine to induce the production of TAP01_04 type antibodies in a person's immune system.

The 'humanized' antibody and the synthetic amyloid-beta vaccination, dubbed TAPAS by the Göttingen team, were subsequently examined in two separate Alzheimer's disease mice models by the researchers. These researchers found that both the antibody and the vaccine helped restore neuron function while increasing brain glucose metabolism, reversing memory loss, and reducing amyloid-beta plaque formation despite not being targeted directly. They used imaging techniques similar to those used to diagnose Alzheimer's in humans.

Because they target a distinct protein, the TAP01_04 humanized antibody and the TAPAS vaccine are pretty different from earlier antibodies or vaccines for Alzheimer's disease that have been evaluated in clinical trials. This makes them very promising as a therapeutic antibody or vaccination for the condition. These promising outcomes have already shown the team's scientific prowess. Patients' life might be transformed if the therapy is effective.

"While the research is in its infancy, if these findings could be duplicated in human clinical trials, it might be transformational," said Professor Mark Carr. "Once Alzheimer's signs are discovered, it may be possible for people to be vaccinated against the illness to prevent it from developing." Currently, researchers are seeking a commercial partner to conduct clinical studies of therapeutic antibodies and vaccination.


Bakrania, P., Hall, G., Bouter, Y. et al. Discovery of a novel pseudo-β-hairpin structure of N-truncated amyloid-β for use as a vaccine against Alzheimer’s disease. Mol Psychiatry (2021).

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