Alzheimer’s vaccine hopes boosted by success in animal trials

Alzheimer’s vaccine hopes boosted by success in animal trials

A VACCINE against Alzheimer’s disease could be a possibility, new research suggests.

US and German scientists recently conducted animal trials to slow down and even reverse the onset of the disease, and the results are exciting.

The experiment manged to reverse memory loss in mice, whose neurological structure is similar to humans.

Scientists behind the breakthrough are keen to move to human trials, but stress that there is more work to be done.

The vaccine trains the immune system to combat a sticky amyloid beta protein that inhibits connections between neurons, and is commonly found in the brain of those with dementia.

The new antibody and vaccine produced by this study target different, soluble forms of the amyloid beta protein, which could be detrimental to healthy braincells.

The researchers adapted an antibody, called TAP01, to ensure the vaccine load is not rejected by the immune system.

They were surprised to find that the protein folded back on itself, forming into more damaging form of amyloid.

Both the antibody and the vaccine restored the brain’s neuron function and increased glucose metabolism in the brain, and results indicated that the mice had restored memory function.

Co-author Professor Mark Carr, of Leicester University, said: “If these results were replicated in human trials, then it could be transformative.

“It opens up the possibility to not only treat Alzheimer’s but also to potentially vaccinate against the disease before the symptoms appear.”

Professor Thomas Bayer, from the University Medical Center Göttingen, said: “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. Some have even shown negative side effects.”

“So, 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”, he concluded.