Losing your mental faculties to a debilitating brain disease such as Alzheimer’s is a huge fear for many older Australians, but scientists hope that they may have found a vaccine for the condition.
A team of UK and German scientists have discovered a new approach to treating Alzheimer’s involving both an antibody-based treatment and a protein-based vaccine that they found reduced Alzheimer’s symptoms in mice.
Alzheimer’s disease is the most common form of dementia in Australia, accounting for around 70 per cent of the more than 400,000 dementia sufferers in the community.
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Rather than focus on the amyloid beta protein in plaques in the brain, which are commonly associated with Alzheimer’s disease, the approach taken by the University of Leicester and University of Göttingen scientists target a different, soluble form of the protein that is thought to be highly toxic.
Scientists have long claimed that shortened or ‘truncated’ amyloid beta plaques are the key to the development and progression of Alzheimer’s disease.
“In clinical trials, none of the potential treatments which dissolve amyloid plaques in the brain have shown much success in terms of reducing Alzheimer’s symptoms,” researcher Professor Thomas Bayer says. “Some have even shown negative side-effects.
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“We decided on a different approach. We identified an antibody in mice that would neutralise the truncated forms of soluble amyloid beta but would not bind either to normal forms of the protein or to the plaques.”
The team then adapted this antibody so that a human immune system would not recognise it as a foreign body and would accept it.
The antibody would then bind to the truncated form of the amyloid beta proteins and they could see the hairpin-shaped structure created as a result.
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Professor Mark Carr, from the University of Leicester, said this allowed he team to engineer this region of the protein to stabilise the hairpin shape and bind to the antibody in the same way.
“Our idea was that this engineered form of amyloid beta could potentially be used as a vaccine to trigger someone’s immune system to make antibodies,” Prof. Carr said.
“It opens up the possibility to not only treat Alzheimer’s once symptoms are detected, but also to potentially vaccinate against the disease before symptoms appear.”
When the team tested the engineered amyloid beta protein in mice, they found that mice who received this ‘vaccine’ did produce antibodies.
The researchers then tested both the ‘humanised’ antibody and the engineered amyloid beta vaccine in two different mouse models of Alzheimer’s disease and they found that both helped to restore neuron function, restore memory loss and reduce amyloid beta plaque formation.
Dr Preeti Bakrania said the findings were significant because the two solutions in this research targeted a different form of the protein to previous antibodies or vaccines.
“This makes them really promising as a potential treatment for the disease, either as a therapeutic antibody or a vaccine,” Dr Bakrania said.
“If the treatment does prove successful, it could transform the lives of many patients.”
Prof. Carr explained that the science is now at a very early stage and the results would need to replicated in human clinical trials before moving to further stages.
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