Hyperactive interferon signaling is a hallmark of trisomy 21 and may contribute to many of the comorbidities associated with Down syndrome.

Distinct intrinsic excitability and synaptic dysfunctions in specific cortical inhibitory circuits lead to abnormal network activity in a mouse model of Down syndrome.

A panel of seven new mouse strains with chromosomal duplications is used to identify a minimal genetic region required in three copies to cause congenital heart defects typical of human Down syndrome.

CA1 physiology is altered in the hippocampus of Down syndrome mice during both spatial exploration and rest, paralleled by an increase in populations of interneurons responsible for single cell and network synchronization.

TcMAC21 is an appropriate “next gen” mouse model for DS research, and provides a proof of concept of using artificial chromosomes to generate non-mosaic humanized animal models of chromosome disorders.

ROBO isoforms with minute sequence variations have significant and distinct functions in axon guidance.

Dosage-compensated gene expression facilitates chromosomal aneuploidy, which presents a rapid route to phenotypic evolution in natural yeast isolates.

Global epigenetic perturbations and accumulation of RNA:DNA hybrids are two novel hallmarks of the lupus-like inflammatory disorder Aicardi-Goutières syndrome.