Aducanumab effective against Alzheimer’s as first drug?


Aducanumab is the new drug that may be the first ever to slow Alzheimer’s disease. It has been approved in the USA – and is highly controversial.

Drug against Alzheimer’s approved in the USA – soon to be approved in Germany?

For Alzheimer’s patients and their families, it is the only glimmer of hope in a desperate situation, for the manufacturer Biogen it is a billion-dollar business – for many scientists and doctors, aducanumab is above all one thing: too little research.

Nevertheless, the U.S. Food and Drug Administration (FDA) granted approval for the novel active substance against Alzheimer’s disease at the beginning of June 2021.

A medical sensation: the active ingredient aducanumab or Aduhelm (U.S. brand name) is the first drug ever to combat the disease itself. In the case of Alzheimer’s dementia, until now only the symptoms could be alleviated with medication, if at all. Now, aducanumab is theoretically expected to slow the progression of mental decline in every Alzheimer’s patient, regardless of stage. A medical revolution? That is highly controversial. That’s not the only reason why it will probably be some time before the drug is launched on the market in Germany – if ever. Read here how the new Alzheimer’s drug works, everything about the research situation, and what makes the aducanumab approval so problematic.

How Alzheimer’s develops and how aducanumab is expected to stop it

Aducanumab is a monoclonal antibody, which means it acts in the body like a kind of vaccination. The goal of a normal vaccination is to create antibodies that act against a pathogen. In the case of Alzheimer’s, it is not viruses or bacteria that are to be fought, but the target is a different one – the protein beta-amyloid. How Alzheimer’s develops and why beta-amyloid plays a major role in it:

For the human brain to be so powerful, more than 100 billion nerve cells work together, constantly processing information and stimuli. For the network to function, the nerve cells are connected via contact points, so-called synapses. Messenger substances enable the exchange of information via the synapses. They are the first to be affected by Alzheimer’s, so that communication between the nerve cells no longer functions properly – the first disturbances become apparent, e.g. increased forgetfulness, concentration and orientation problems.

In the further course of the disease, nerve cells then die completely, they are irretrievably lost. This leads to drastic symptoms, which can be very individual depending on the Alzheimer’s patient – even how quickly the disease progresses varies greatly. Alzheimer’s progresses in four stages, which can last up to 20 years. In the third and fourth stages, those affected often suffer from, among other things:

  • Loss of short-term memory and disturbance of long-term memory, e.g., with abrupt memories from childhood.
  • Loss of ability to recognize faces, even of close relatives.
  • Disturbed sense of time and disturbed day/night rhythm.
  • Disorientation, nervousness, distrust, frequent need to run away.
  • Speaking, swallowing and movement become difficult or impossible.

In short, the brain gradually stops functioning. But what destroys this once powerful organ? Despite intensive research, it is still not known exactly why some people develop Alzheimer’s and others do not. What is certain, however, is that two factors lead to the destruction of nerve cells: the protein beta-amyloid and the protein building block tau protein.

Beta-amyloid occurs naturally in the brain and is in itself completely harmless. Beta-amyloid results from a biochemical reaction. In Alzheimer’s disease, this process changes, resulting in damaged beta-amyloid proteins. They accumulate and clump together, forming insoluble deposits between the nerve cells, the plaques. In addition, there is an altered tau protein, a protein building block, in the nerve cells.

Tau proteins help transport nutrients from one cell to another. In Alzheimer’s, the tau protein changes so that it is deposited in the nerve cell, causing it to lose its shape and decay.

Alzheimer’s, then, stems from nerve cells in the brain being damaged by protein deposits. This is where aducanumab comes in. The active ingredient reduces the plaques of the protein beta-amyloid in the brain, as studies have clearly shown. There is a great deal of disagreement about everything else.

Why the approval of the Alzheimer’s drug is so controversial

It was an unusual move by the U.S. Food and Drug Administration (FDA) – it has now granted marketing approval to aducanumab, but only on the condition that further research takes place. Normally, all studies and tests with patients must be completed before a new drug can be marketed. However, the situation in the treatment of Alzheimer’s is complicated, not to say desperate. Better to have a drug that only perhaps prevents patients from deteriorating further than to have no drug at all, is the argument of patient representatives and Alzheimer’s patients. In addition, precious time should not be wasted. After all, even aducanumab is not capable of curing Alzheimer’s or reversing the damage; the disease can only be prevented from progressing – maybe.

How effective aducanumab really is is highly controversial and cannot yet be determined with certainty. That’s because it’s not clear whether reducing beta-amyloid is really enough to stop Alzheimer’s. Clinical trials by the manufacturer, Biogen, do not show a clear picture, but rather two contradictory phase 3 studies. In pivotal trials, phase 3 is a study with a large number of patients, one group of whom receives the new drug and another group treated as usual or given a placebo drug. The comparison of results is intended to show whether the drug is effective and also what side effects occur. In the case of aducanumab, a phase 3 study showed that the drug was able to slightly slow mental decline in Alzheimer’s patients. Another study, however, showed no clear effect. As a result, the trials were stopped prematurely because aducanumab did not appear to have any benefits for sufferers – it was unethical to continue exposing people to a novel drug with potential side effects if it would not help anyway.

However, the manufacturer Biogen then explained that it had evaluated further data and found that a particularly high dose of aducanumab did have positive effects. The decline in mental abilities and memory is said to have been slowed down by about 22 percent. This means that the mental decline, calculated over a period of one and a half years, could be postponed by about four months. After much debate among various scientific bodies, the FDA has now decided to approve the drug in order to give Alzheimer’s patients and their families the chance to spend more time in better health.


Leave A Reply