Research on Alzheimer's vaccine shows great promise

A team of U.K. and German scientists are seeing some success in a potential breakthrough in Alzheimer’s treatment.

Liz Braun, Toronto Sun 3 minute read November 18, 2021

A team of U.K. and German scientists are seeing some success in a potential breakthrough in Alzheimer’s treatment.

The team’s research, originally published in Molecular Psychiatry, shows the antibody-based treatment and the protein-based vaccine they developed reduced Alzheimer’s symptoms in mice.

Involved scientists are at the University of Leicester, the University Medical Center Göttingen and the medical research charity LifeArc.

Rather than focus on the amyloid-beta protein in plaques in the brain that are associated with Alzheimer’s, the antibody and vaccine both target a different soluble form of the protein, that is thought to be highly toxic, according to Science Daily.

(Much of the work against Alzheimer’s is focused on reducing amyloid, which accumulates in the brain of those with dementia, but reducing amyloid doesn’t always reduce symptoms.)

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

In Alzheimer’s disease, a high proportion of these string-like molecules become shortened or ‘truncated’ and some scientists now think that these forms are key to the development and progression of the disease.

Working with mice, the scientists identified an antibody that would neutralize the truncated forms of soluble amyloid-beta, but would not bind either to normal forms of the protein or to the plaques.

From the antibody and an engineered form of amyloid beta-protein they developed a potential new vaccine that prompts the immune system to respond appropriately; moreover, further testing on mice showed hopeful results in restored neuron function and restored memory loss.

The University of Toronto’s Dr. Carmela Tartaglia (Marion and Gerald Soloway Chair in Brain Injury and Concussion Research) is a specialist in Neurodegenerative Diseases and she is cautiously optimistic about the new research.

It is, she said in a recent interview, “A novel approach, as they aren’t targeting plaque, but another form of amyloid — and that might be a better approach before it sticks to the brain. There’s validity in what they’re doing.”

But, she adds, “It’s in mice. And we’ve cured it in mice before. Obviously, we don’t have a cure yet, so we keep our minds open. But many therapies that eventually failed showed promise in mice.”

Mice don’t get Alzheimer’s, explained Tartaglia, except in the lab. “So the Alzheimer’s we give them can be helped by this approach.”

Nonetheless, she remains optimistic about the new findings — “it is a new avenue” — and notes with dry humour that optimism is crucial in her field.

She works on neurodegenerative diseases, so she sees people with Alzheimer’s and with many other forms of cognitive impairment, caused by such things as multiple concussions or long COVID.

Dr. Tartaglia is one of the scientists engaged in a global consortium of specialists working on the connection between long COVID and dementia.

“The issue is that long COVID seems to be a risk for accelerating neurodegenerative decline. Some people do get better, but it takes a long time.”

She is seeing patients in their 30s and 40s, some of whom had very mild COVID and never went to hospital, but still struggle 18 months later.

“They still can’t go back to work, can’t sleep, and have constant headaches,” she said.

Tartaglia doesn’t want to alarm people who have persistent COVID symptoms.

“But believe me, you don’t want this. Let me stress the importance of being vaccinated,” she said.