A drug project, on a track still little explored, has just recorded interesting results against Alzheimer’s disease, even if it is far too early to be enthusiastic.
This is perhaps a breakthrough in the search for a treatment against Alzheimer’s disease, which has been stalling for twenty years. ” These results […] are particularly encouraging and represent a first in several respects ”, welcomes Andrea Pfeifer, boss of the start-up AC Immune which is developing, together with a subsidiary of the Swiss pharmaceutical giant Roche, a treatment against 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 – follows a track that has not yet been explored in the search for an anti-Alzheimer’s treatment, an area where failures have been increasing for twenty years.
AC immune and Roche have explored a new avenue: acting on the abnormal behavior of Tau proteins, present in neurons. In patients, they aggregate in clusters which end up leading to the death of the cell. The two laboratories have developed 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 remain very careful: there is clearly a marketing side, advertising effects (even if) can really be something”, nuances the neurobiologist Luc Buée, specialist in diseases linked to Tau .
This 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.
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 the neurobiologist Florence Clavaguera, specialist in the protein of Tau. 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.