Estrategias farmacológicas para paliar los déficits cognitivos en el síndrome de Down
Year: 2017
Type: dissertation
Abstract: Down syndrome (DS), the most common genetic cause of intellectual disability, is due to the total or partial triplication of human chromosome 21. Despite numerous efforts, the mechanisms whereby gene triplication leads to the different DS phenotypes have not been elucidated and there are no pharmacological treatments available for the cognitive alterations in DS. Over the last years, the most accepted murine model of DS, the Ts65Dn mouse, has been widely used to investigate the neural mechanisms underlying the intellectual disabilities of DS individuals. Furthermore, a number of pharmacological therapies have been shown to partially restore neuromorphological anomalies concomitantly with cognition in these mice. This review is focused on the major alterations found in the brains of DS individuals and of mouse models of this condition. Information from the preclinical evaluations in the Ts65Dn mouse and state of human clinical trials performed in individuals with DS are also summarized. In the second part of this work, the methods used in the preclinical assessment performed during my stay in the Laboratory of Neurobiology of Learning of the Department of Physiology and Pharmacology of the Faculty of Medicine of Santander are described.
Source: UCrea (University of Cantabria)
Authors: Suárez Méndez, María Paz
Language: Spanish
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2752393504