And again failure
Two Alzheimer's drugs failed in Phase Three clinical trials
However, experts still want to continue researching one of them
Neurophysiologists have summed up the results of the third phase of clinical trials of gantenerumab and solanezumab – promising drugs for Alzheimer's disease. Both drugs failed to stop the extinction of memory and mind in volunteers, the researchers write in the scientific journal Nature Medicine (Salloway et al., A trial of gantenerumab or solanezumab in predominantly inherited Alzheimer's disease).
"Our results indicate that neither drug had a beneficial effect on the cognitive abilities of the volunteers, however, both substances were combined with beta-amyloid. We plan to continue experiments with gantenerumab, whose molecules did not cause negative changes in the condition of patients, whereas solanezumab accelerated the extinction of their memory," the researchers write.
Now biologists suggest that the main sign and possible cause of the development of Alzheimer's disease is the accumulation of so-called beta-amyloid, a pathogenic protein inside brain cells. It is fragments of the APP protein, which plays an important role in the formation of connections between neurons. Similarly, the concentration of damaged molecules of another substance, tau protein, increases in brain cells.
Over the past two decades, chemists and biologists have discovered about three dozen compounds that slow down the accumulation of pathogenic forms of APP and tau protein in single brain cells. Many of these drugs successfully prevented the development of Alzheimer's disease in experiments on mice and other animals, but subsequent clinical trials in all cases ended in failure.
An international team of neurophysiologists led by Randall Bateman, a professor at Washington University in St. Louis (USA), added two more drugs to the number of such failures - gantenerumab and solanezumab. Both of these substances are antibodies capable of attaching to beta-amyloid molecules in its two main forms.
According to scientists, 52 volunteers who suffered from a hereditary form of Alzheimer's disease resulting from the appearance of mutations in the genes of the PSEN family or in some other DNA sites participated in the second and third phase of clinical trials of gantenerumab and solanezumab. Carriers of such "typos" in the genome are almost guaranteed to become victims of dementia in 40-50 years.
This makes them ideal participants in clinical trials to test the effectiveness of Alzheimer's drugs that prevent or inhibit the accumulation of beta-amyloid and tau protein in their neurons. Enlisting the support of volunteers, the scientists divided them into three groups, two of which received injections of one of the antibodies, and the others – a placebo. The second phase of testing began in 2012, but in 2015 it was extended and carried out together with the third phase for the next four years.
Recently, scientists summed up these observations by comparing how the state of the brain and cognitive abilities of volunteers in all three groups changed. In general, both drugs failed to pass the third phase of testing – gantenerumab and solanezumab could indeed combine with beta-amyloid molecules, but they did not prevent the memory and mind of the participants of the experiment from fading in any way.
Moreover, the observations of Professor Bateman and his colleagues indicate that solanezumab not only did not protect the participants of the experiment from Alzheimer's disease, but also accelerated the development of dementia compared to how the condition of the volunteers from the control group changed. For this reason, neurophysiologists refused to conduct further experiments with this antibody.
Subsequent observations and experiments, the researchers hope, will help them understand why gantenerumab actively removed beta-amyloid from the brain cells of the participants in the experiments, but did not help them protect themselves from the extinction of mind and memory. According to the researchers, this may be due to the initially low dose of antibodies and the slow rate of its build-up, which scientists plan to check in the near future.
Portal "Eternal youth" http://vechnayamolodost.ru