Torres, Eduardo Martin PHD

The central view of Down syndrome research is that pathologies in patients are driven by the increased expression and activity of genes present on chromosome 21. However, it has proven very difficult to show that an extra copy of a specific gene is solely responsible for a given phenotype in Down syndrome. In this project we aim to elucidatethe cellular defects associated with trisomy 21 caused by the disruption of cellular homeostasis due to the presence of the extra chromosome independent of the identity ofgenes encoded in chromosome 21.