Reacción a "EMA recommends not approving donanemab for Alzheimer's"

In 1999, Schenk and colleagues published an encouraging paper in Nature reporting that immunisation with beta-amyloid in genetically modified mice that developed deficits similar to those caused by Alzheimer's disease in humans reduced the impact of the disease in the animals, even improving certain cognitive abilities in the treated animals. This methodology was tested in humans and, while certain results were encouraging, there were also a number of cases where immunisation resulted in serious cerebrovascular problems. In other words, while it may have worked, the therapy could cause more damage than it was intended to repair.

Since then, work has been ongoing on various alternatives and modifications of such therapies to maintain, or enhance, the beneficial effects of this immunisation while trying to avoid the more severe side effects. In recent months, similar products have been deauthorised and then authorised for use, the most prominent being lecanemab, which was not authorised initially but was later found to be somewhat effective in a particular group of patients.

In this case, as with lecanemab, the European agency, which carries out an independent analysis of the results of clinical trials, does not agree with the conclusions of its US counterpart, the FDA, and considers that the use of donanemab poses a high risk of cerebrovascular problems with a very slight improvement in the symptomatology of Alzheimer's disease. On the previous occasion, the EMA did follow the FDA's lead and authorised the use of lecanemab in patients for whom it was not contraindicated. It remains to be seen whether Eli Lilly has data that could lead to a similar change in the near future, although it would be surprising if they had not already presented it.