Brian F. Niemeyer

This study shows that increased mitochondrial metabolism in Down syndrome iPSCs impairs neuroectoderm commitment by reducing ciliation, and this effect can be reversed by inhibiting mitochondrial calcium uptake.

This study identifies hyperactive interferon signaling and lymphoid tissue disorganization as drivers of adaptive immune dysfunction in Down syndrome across development and aging.

This study identifies attenuated estrogen signaling and NRIP1 as key factors in trophoblast defects in Down syndrome using patient-derived stem cells.

The paper reports altered hepatic metabolism in Down syndrome using multi-omic analysis of plasma and mouse models, showing increased bile acids and liver dysfunction that can be modulated by diet.