Similar means from other companies have so far hardly shown any real improvements in the everyday life of those affected. But don’t write off the funds just yet.
This image shows the devastating nerve damage in the brain of an Alzheimer’s patient (left). It’s downright shrunken compared to a healthy person’s brain.
For Alzheimer’s patients and their families, there is once again one less hope. On Monday, the Swiss pharmaceutical company Roche announced that its drug called Gantenerumab against the fatal brain disease had shown no effect in clinical studies.
The exact results will not be presented at a congress until the end of November. But this much is already known: the decline in mental abilities was only slowed down by 6 to 8 percent. Almost 2000 subjects were observed for 27 months.
Dissolve toxic clumps of protein in the brain
A slowdown in mental degradation by the values mentioned does not mean any improvement in the everyday life of dementia patients. For comparison, drug companies Biogen and Eisai recently announced their drug had achieved a 27 percent slowdown. Even this was only slightly noticeable in everyday use. And nota bene, only the progression of dementia is slowed down, it is neither stopped nor cured.
All the drugs mentioned are based on the same principle of action. These are antibodies that dock to special protein clumps in the brain. These clumps are called amyloid plaques in technical jargon. The antibodies mentioned should now dissolve these clumps.
Such lumps are found in large numbers in the brains of Alzheimer’s patients, but also in patients with another form of dementia. Numerous cell culture and animal experiments have shown that the clumps are toxic to nerve cells. As a result, amyloid plaques became the focus of Alzheimer’s research and drug development more than fifteen years ago.
It is true that no one can currently say with certainty whether these amyloid clumps are the cause of dementia. However, the majority of experts assume that the lumps play an important role in the course of the disease.
When asked on Monday, Roche explained the poor performance of its antibody by saying that it had not managed to clear enough clumps of protein in the brain. This could be because not enough antibodies arrived in the brain. Because the Roche substance was injected under the skin. The anti-clumping antibodies of the competing companies, on the other hand, are injected directly into the bloodstream. Roche is now hoping for a better effect from a variant of the antibody drug that reaches the brain better and faster.
However, a fundamental problem with antibody therapy in dementia is that it cannot achieve a cure. Even in the best of cases, the antibodies only dissolve the clumps. However, the deficits that have already occurred are not repaired, i.e. nerve cells that have died are not regenerated, and the holes that have arisen in the neural network are not plugged again.
An antibody cannot do that at all. Nobody currently knows whether it would even be possible to specifically stimulate the formation of new nerve cells in the brain. Not to mention how it could be possible for these to fit precisely into the holes and interweave with the nerve cells that are still there.
Substances that prevent the formation of toxic amyloid plaques or dissolve them and thus slow down the progression of nerve loss are currently the only therapy option. And that’s why it’s so important to research it.
Are the funds given far too late?
But experts agree: the antibodies have to be administered very early on. As soon as the first clumps of protein form – and thus long before those affected show the first symptoms of dementia. Nowadays it is assumed that the degradation of the nerve cells starts up to ten years before the first symptoms of dementia appear.
Scientists and doctors have therefore been calling for more research into the whistleblowers, so-called biomarkers, for dementia. These whistleblowers are also extremely important for other diseases: we know that high blood pressure, elevated blood lipid levels, obesity or certain gene variants increase the risk of a heart attack. Anyone who has these risk factors is closely monitored and, if necessary, treated with medication. In the case of Alzheimer’s disease and other forms of dementia, too, risk factors and risk patients must be identified urgently.
It could well be that all of the antibodies mentioned, as well as others still in development, against protein clumps are quite effective tools. But that they are currently being administered at the wrong time. The worst case scenario for sufferers and their families would be that eliminating protein clumps has little effect on the onset or progression of Alzheimer’s or any other form of dementia, and thus all those antibodies are useless.