New study suggests Alzheimer’s could be vaccinated against

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A new approach has been developed by scientists for a possible treatment of Alzheimer’s disease and vaccination against it.

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The study shows that both the antibody-based treatment and the protein-based vaccine developed by the team reduced Alzheimer’s symptoms in a mouse model of the disease.

Rather than focusing on the amyloid beta protein in plaque in the brain, which is commonly associated with Alzheimer’s disease, both products target a different form of the protein, which is known to be highly toxic.


The amyloid beta protein naturally exists in solution as highly flexible, string-like molecules, which can join together to form fibers and plaques.

A high proportion of these molecules become shortened in Alzheimer’s, and some scientists now think that these forms are important for the development and progression of the disease.

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The work is a collaboration between researchers from the University of Leicester, the University Medical Center Göttingen and the medical research charity LifeArc.

Professor Thomas Baer, ​​from the University Medical Center Göttingen, said: “In clinical trials, none of the potential treatments that dissolve amyloid plaques in the brain have shown much success in reducing the symptoms of Alzheimer’s.

“Some have even shown negative side effects. So we decided on a different approach.

“We have identified an antibody in mice that will neutralize the truncated forms of soluble amyloid beta, but will not bind to normal forms of the protein or to plaques.”

This antibody was adapted by Dr. Preeti Bakkarnia and colleagues at LifeArc, so a human immune system would not recognize it as foreign and would accept it.

The Leicester researchers were perplexed when they discovered how and where this humanized antibody, called TAP01-04, bound to the short form of amyloid beta.

They observed that the amyloid beta protein folded back on itself, into a hairpin-shaped structure.

Professor Mark Carr, from the Leicester Institute of Structural and Chemical Biology at the University of Leicester, explained: “This structure had never been observed before in amyloid beta.

“However, the discovery of such a definite structure allowed the team to stabilize this region of the protein the shape of the hairpin and bind to antibodies in the same way.

“Our idea was that this engineered form of amyloid beta could potentially be used as a vaccine to trigger one’s immune system to make TAP01-04 type antibodies.”

When the engineered amyloid beta protein was tested in mice, they found that the animals that received this “vaccine” produced antibodies of the type TAP01.

This antibody and the engineered amyloid beta vaccine, called TAPAS, were tested in two different mouse models of Alzheimer’s disease.

Based on the imaging techniques used to diagnose Alzheimer’s in humans, the researchers found that both the antibody and the vaccine helped restore neuron function.

They also helped restore memory loss, boosting glucose metabolism in the brain, and while they weren’t directly targeted, they also reduced amyloid beta plaque formation, according to the study.

Dr Bakrania of LifeArk said: “The TAP01-04 humanized antibody and TAPase vaccine are very different from previous antibodies or vaccines for Alzheimer’s disease that have been tested in clinical trials, as they target a different form of the protein. We do.

“This makes them really promising as a therapeutic antibody or a potential treatment for disease as a vaccine.

“The results so far are very exciting and testament to the scientific expertise of the team.

“If the treatment proves successful, it could change the lives of many patients.”

Prof Carr said: “While the science is still in its early stages, if these results were to be replicated in human clinical trials, it could be transformative.

“This opens up the possibility of not only treating Alzheimer’s once symptoms are detected, but also potentially vaccinating against the disease before symptoms appear.”

Researchers are now looking for a commercial partner to take therapeutic antibodies and vaccines through clinical trials.

The findings are published in Molecular Psychiatry.

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