The disruption of gene transcription and cell function in Down syndrome is very similar to that seen in cellular aging, MIT scientists find. They used anti-senescence drugs to correct the errors in cell cultures, establishing senescence as a potentially targetable mechanism for future treatment.
MIT scientists show that the extra copy of chromosome 21 in Down syndrome disrupts the 3D-genome, epigenome, and transcriptome of neural progenitor cells such that they resemble aged cells. The molecular changes result in functional deficits in cell proliferation and migration in the trisomy 21 bearing developmental cells. Treatment of patient-derived neural progenitor cells with a senolytic drug combination consisting of dasatinib and quercetin ameliorates these disruptions.
February 17, 2021
by Jeanna Lucci-Canapari
A multi-institution symposium led by Yale School of Medicine treated more than 1,900 online participants from across the country to a showcase of research from a diverse group of talented postdoctoral researchers, with the goal of propelling their promising careers in scientific discovery. The Intersections Science Fellows Symposium was held through Zoom sessions and webinars from January 6 through 8, and was hosted by a coalition formed by Yale and 25 other national research institutions.
The symposium featured the research contributions from 26 junior scientists, who were chosen to present their work as 2021 Intersection Science Fellows. Selected from a pool of more than 400 applicants, the fellows largely represented communities that have been historically unrepresented in the field of medical research, including those from ethnic and racial minorities, those with disabilities, those from low socioeconomic backgrounds, women, or those