Dhe number of Alzheimer’s cases is increasing. However, despite intensive research, the disease has not yet been cured and the mechanisms by which it develops are controversial. The so-called amyloid hypothesis states that the protein amyloid is the trigger by forming clumps in the brain, so-called plaques. As early as 1992, researchers, including the biochemist Christian Haass, demonstrated that we all produce amyloid throughout our lives. Others, however, see this as proof that the amyloid hypothesis cannot be correct – otherwise why doesn’t every one of us get Alzheimer’s? But it’s not that simple: According to Haass, it’s just a matter of time and genetics how long it takes for the disease to break out – or if it breaks out at all.
Now the amyloid hypothesis has received new impetus: A few weeks ago, the pharmaceutical companies Eisai and Biogen published parts of the results of a study in which 1,795 patients were examined for the effects of the amyloid antibody lecanemab. The result: The plaques decreased significantly and the decline in cognitive abilities was 27 percent slower than in the placebo group over the 18-month treatment period. The antibody aducanumab previously tested by Biogen was not approved by the European Medicines Agency. Other antibodies, including donanemab, are still in the testing phase.