Alzheimer's: New active ingredient cleans up the brain

Christiane Fux studied journalism and psychology in Hamburg. The experienced medical editor has been writing magazine articles, news and factual texts on all conceivable health topics since 2001. In addition to her work for, Christiane Fux is also active in prose. Her first crime novel was published in 2012, and she also writes, designs and publishes her own crime plays.

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A new Alzheimer's drug has shown itself to be surprisingly effective in initial tests. With the help of an antibody, it has been possible to dissolve clumped proteins in the brain, which are typical for dementia. It seems particularly promising that this actually slowed the mental decline of the patient. But is this really the breakthrough?

Aducanumab is the name of the active ingredient that raises hopes. Right? One thing is certain: it binds to the so-called beta-amyloid plaques that accumulate in the brains of Alzheimer's patients. When aducanumab is administered, the protein accumulations marked in this way are eliminated by immune cells.

Degraded Alzheimer's plaques

After promising experiments with mice, the researchers led by Roger M. Nitsch from the University of Zurich had now tested the active ingredient on 165 patients at an early stage of the disease. For this purpose, the participants received a monthly infusion of aducanumab or a placebo over a period of around one year. In test subjects who had received the highest dose of the antibody, the plaques subsequently reduced to an almost normal level. This is because the accumulations in the brain are also found in healthy people, but they are normally constantly being broken down again.

Slowed down performance

The effect on mental abilities was particularly encouraging. "While the mental deterioration progressed significantly in patients in the placebo group, the cognitive abilities in patients who had received the antibody remained significantly more stable," says Nitsch.

That sounds great at first. The big problem with Alzheimer's is still: It is still completely unclear whether the plaque accumulations actually cause the brain cells to die and thus cause symptoms of dementia. This is a widespread hypothesis, which is also strengthened by the study results. However, it can still not be ruled out that plaque formation is only a side effect of Alzheimer's disease and is not at all responsible for the symptoms of dementia.

Long-term effectiveness still unknown

After the first test, it remains unclear how well the remedy works in the long term - and whether it could stop the disease or even reverse it. A much larger long-term study with 2,700 participants should now clarify this.

In fact, there have always been promising therapeutic approaches in the past that later disappointed on a large scale.

Alzheimer's nerve disease

In people with Alzheimer's disease, in addition to the plaques that can be broken down by aducanumab, bundles of modified so-called tau proteins also form in the brain. These processes begin long before the first signs of dementia appear. Over time, nerve cells die, which means that not only memory but also language, orientation and thinking skills and ultimately the patient's personality decline.

To date, neither the triggers of the disease nor the exact mechanisms are known - there is also no effective causal therapy available. So far, cognitive abilities can only be improved in the early phase of the disease with the help of medication for a certain period of time.

Almost 1.6 million people with dementia currently live in Germany, two thirds of whom suffer from Alzheimer's. Since the likelihood of falling ill increases with age and people get older, the number of Alzheimer's patients is also steadily increasing. Women who have a longer life expectancy are more likely to fall ill than men. For the year 2050, researchers expect the number of dementia to almost double.

Source: Jeff Sevigny: The antibody aducanumab reduces Aß plaques in Alzheimer's disease; Nature 537, 50-56 (September 01, 2016) doi: 10.1038 / nature19323

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