Autor/es reacciones

Jesús Flórez

Professor of Pharmacology at the University of Cantabria and President of the Ibero-American Down21 Foundation

There is a hypothesis, in principle plausible until proven otherwise: the possible positive action of the GnRH system on cognition (in addition to the known endocrine actions). The study aims to confirm this hypothesis and, at the same time, to demonstrate the benefit it could bring to the manifestations of cognitive impairment in people with Down's syndrome. 

The preclinical study focuses on the Ts65Dn mouse, one of several murine models of Down's syndrome. It has been the most widely used so far, but is far from the perfect model (Klein JA and Haydar TF (2022) and Drug Therapy: Neurodevelopment and Neurodegeneration in Down Syndrome). 

The studies carried out by the authors in this model with regard to the development of the GnRH system are complex and demonstrative in their various aspects. I consider the experimentation on cognition in the mouse to be somewhat weak. 

There are dozens of products already tested in the Ts65Dn mouse which, having sometimes substantially improved brain function and cognitive tests in this model, have subsequently failed when the experimentation was transferred to people with Down's syndrome. Hence the need to always test in other models. 

The clinical trial is very tentative and lacks the conditions required to show positive effects objectively. It should have been double-blind and compared with placebo, and with a larger number of subjects. I am surprised that Science has accepted that part of the work. 

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