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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.