Drugs for Alzheimer’s: A breakthrough?

Drugs for Alzheimer’s
Is the breakthrough in the treatment of Alzheimer’s now coming?

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It’s been a long time coming: a drug that helps against Alzheimer’s. Now there are actually two new means. Are they the breakthrough?

There are few illnesses we fear as much as one dementia – and only a few keep medicine in such suspense. For example, while many cancers can now be treated well, the search for Medicines against the great forgetting have a long history of disappointments. A drug that gave hope was last approved over 20 years ago. Memantine is still part of the standard medication along with cholinesterase inhibitors and ginkgo, but all three approaches only achieve a slight improvement for those affected.

Then at the beginning of 2023 Glimmer of hope: A new drug is coming onto the US market and another has been submitted for approval. Lecanemab, which will probably also be approved in our country soon, and donanemab are so-called anti-amyloid antibodies and reduce protein deposits in the brain, which are considered a possible cause of the disease. People with Alzheimer’s who took lecanemab performed better on tests of memory and orientation than those in the placebo group after a year and a half of therapy. The progression of the disease was slowed down by almost a thirdannounced the manufacturers.

Small steps on the way to your goal

Sounds good, but it is put into perspective when you look at the absolute numbers: on a scale from 0 to 18 the symptoms only improved by half a point. The delay in illness is given as five to seven months. Donanemab seems to work a little better, but still not enough, says Linda Thienpont, scientific director of the Alzheimer’s Research Initiative: “For a drug to be successful, the symptoms should improve significantly and become noticeably fewer. The new active ingredients cannot promise that either. “

So much ado about nothing? It’s not that easy; Small steps also count in the treatment of Alzheimer’s. Precisely because the causes of dementia are not fully understood, the medications are more like experimental balloons than reliable breakthroughs.

Alzheimer’s begins silently.

Most researchers assume, for example, that proteins such as beta-amyloid plaques and tau fibrils – these are fibers inside cells – damage nerve cells. But inflammatory reactions in the brain also seem to play a role. What scientists agree on is that until now, medications have simply been applied too late in the disease process. “Alzheimer’s begins silently. The disease only becomes apparent 20 to 30 years after the degradation process has begun and many of the nerve cells have already been lost,” explains Linda Thienpont. The brain can compensate for the loss for a very long time. If dementia becomes noticeable through problems with memory or orientation, these are degenerative processes is already well advanced and no drug can bring dead nerve cells back to life.

The dilemma

In order to prevent dementia before it breaks out, you need, above all, sensitive people Detection methods. Through eye examinations, biomarkers in the brain fluid and blood or using immune cells, Alzheimer’s can now be traced back almost to its beginnings – but none of the tests have yet made it to the market.

So it could be that the new drugs work better – but just only in a very early stage of the disease. So early that the disease is usually not even recognized yet. A dilemma.

In addition: Therapy with the new medications is not that easy to carry out. Patients must be monitored closely because in very rare cases there is a risk of brain swelling and microbleeds. Imaging procedures using MRI are suitable for this – a costly affair in the long run. The medication also needs to be injected every few weeks.

So the search continues

The German Association of Research-Based Drug Companies currently lists 24 drugs that are being tested on those affected. In addition to other amyloid antibodies too new approaches, such as those that improve signal transmission between nerve cells or increase the cells’ energy metabolism. “The exact process of destruction in the brain is obviously something very individual,” says Linda Thienpont. “We therefore need combination therapies that are individually tailored to those affected. The antibodies will definitely be useful for this, but they are not a panacea.”

But there is also a great opportunity in prevention. Studies show that in some developed countries the rate of new cases has decreased over the past two decades. This could be due to better living conditions and healthier aging, for example because known risks such as diabetes or high blood pressure are avoided or consistently treated. Linda Thienpont is confident: “Through our lifestyle alone, we can reduce the risk of Alzheimer’s by up to 40 percent.”


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