Mice with a mutation that disrupts the release of growth hormone show greatly increased lifespan, which can be further increased by caloric restriction.

Membrane potential recordings in awake mice from two genetically defined classes of neocortical inhibitory neurons reveal their distinct patterns of activity and unitary excitatory synaptic inputs, which are differentially modulated by behavior and local network activity.

Genome sequencing of mice selected for longer limbs reveals that rapid selection response is due to both discrete loci and polygenic adaptation.

Three months treatment with the drug rapamycin increases lifespan, alters cancer prevalence, remodels the microbiome, and improves functional measures of health in middle aged mice in a dose- and sex-dependent manner.

During natural visual behavior in mice, orienting towards a target is driven by head movements, during which the eyes stabilize and shift the visual input.

Reduced expression of a single transcription factor is sufficient to improve fitness and health at old age and increases the lifespan in female mice.

Mirroring human patients with ARID1B mutations, Arid1b haploinsufficient mice exhibited numerous neuropsychiatric defects and revealed IGF1 deficiency related growth impairment that could be ameliorated with growth hormone supplementation.

Social-interaction impairment in germ-free mice is associated with a markedly altered transcriptional response to social novelty in the amygdala, as characterised by replacement of upregulation of common stimulus-induced pathways with upregulation of the splicing machinery.

A tumor-specific regulatory region has been identified upstream of the Myc oncogene.

The dramatic extension of lifespan in Sirt6-deficient mice by Trp53 haploinsufficiency suggests that SIRT6 has distinct biological function from SIRT1 in regulating p53 activity and preventing cells from senescence/apoptosis.