Alzheimer’s: a new hope, shy, to treat the disease – Orange news

AFP, published on Tuesday, September 21, 2021 at 8:24 p.m.

This is perhaps a breakthrough in the search for a treatment against Alzheimer’s disease, which has been stalling for twenty years. A drug project, on a track still little explored, has just recorded interesting results, even if it is far too early to be enthusiastic.

“These results (…) are particularly encouraging and represent a first in several respects”, welcomes AFP Andrea Pfeifer, boss of the startup AC Immune which is developing, together with a subsidiary of the Swiss pharmaceutical giant Roche, treatment for Alzheimer’s disease.

The two groups are in the process of evaluating its effectiveness and announced the first favorable results at the end of August, which however have yet to be published in detail and reviewed independently.

If the announcement is interesting, it is because this molecule – semorinemab – is following a track that has not yet been explored in the search for an anti-Alzheimer’s treatment, an area where failures have been increasing over the past twenty years.

This has, in fact, focused on the destruction of plaques formed by certain proteins, called beta-amyloids, in the brain of patients. By compressing neurons, they are one of the two major factors in Alzheimer’s disease.

But this track has given few results, with the exception of a treatment of Biogen authorized this year by the American health authorities, without unanimity on its therapeutic interest.

For several years, laboratories have therefore sought to act on the second factor that characterizes Alzheimer’s disease: the abnormal behavior of another category of proteins, called Tau, which are present in neurons. In patients, they aggregate in clusters which end up leading to the death of the cell.

It is in this direction that AC Immune and Roche have gone. It is a synthetic antibody which must recognize these clusters in order to destroy them.

– No miracle treatment –

This treatment has been given for almost a year to patients with relatively advanced Alzheimer’s disease. In the end, according to both groups, the decline in their cognitive abilities – assessed using standardized tests – was almost half that of those who received a placebo.

This is the first time that such a positive result has been announced for a treatment project targeting Tau, after a series of failures including, this year, another project from Biogen.

However, “I would still be very careful: there is clearly a marketing side, advertising effects (even if) can really be something”, nuance with AFP the neurobiologist Luc Buée, specialist diseases related to Tau.

First, it is only an early trial, called phase 2, with a limited number of patients. To confirm the effect of the treatment, it will be necessary to enter the next phase, potentially with thousands of people tested.

Calling himself a “scalded cat”, Mr. Buée recalls that a number of projects following the beta-amyloid track had given good results in phase 2, before turning out to be disappointing in the next stage.

Above all, the results of semorinemab remain mixed. Cognitive testing is much better in patients who received it, but there is no difference in their behavior in real life, which is called functional decline.

In other words, “it is promising and frankly it is positive, but it does not cure yet”, underlines to AFP the neurobiologist Florence Clavaguera.

How to explain this difference in results? Ms. Clavaguera, as indeed AC Immune, puts forward a hypothesis: functional decline takes longer to be felt and there may be a difference in several months, the treatment trials continue to run their course.

But nothing currently allows us to be sure. And, even if semorinemab confirms its interest, it is certainly unrealistic to hope that a single miracle treatment will appear to cure Alzheimer’s disease.

“It will ultimately be necessary to combine the two approaches, an anti-Tau treatment and an anti-beta (amyloid) treatment,” warns Ms. Clavaguera. “In all cases of Alzheimer’s disease, there are two proteins that are pathological.”