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.

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.

Environmentally-mediated gene induction is extended beyond the duration of an external cue by sustaining a nucleosome-depleted chromatin structure.

A machine-learning approach is used to predict 1.35 million interactions for 85% of the human proteome.

Delayed intramuscular gene therapy with neurotrophin-3 after corticospinal tract injury reduces spasticity and improves locomotion by treating underlying causes of spasticity.

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.

A novel transposon-based enhancer trap screen in mice permits high throughput development of highly restricted driver strains targeting specific neuronal cell types.

Serum amyloid A proteins bind retinol with nanomolar affinity, and do so by forming oligomers that create a hydrophobic pocket that shields retinol from the aqueous environment.

The transcriptional response of human neurons to calcium ion signals shows evolutionary divergence from those responses elicited in mouse neurons, providing evidence in favour of using human systems to study neuronal responses to external stimuli.

SAA removes toxic products of lipolysis of the cell membrane by sPLA₂, indicating that SAA and sPLA₂ act synergistically to clear debris from injured sites, as required for tissue healing.