Comparative transcriptomics of whole blood can be used to evaluate the systemic host response and its concordance between human and mouse malaria and aid the selection of appropriate models for translational malaria research.

Hypersynchrony in a mouse model of Rett syndrome impairs ripple-dependent memory consolidation and leads to a decrease in experience-dependent refinement of place cell activities.

AAV-Txnip prolongs vision in mouse models of blindness, enhancing lactate catabolism, mitochondrial health, and ATP production in a condition that likely has a limited glucose supply.

Impairing TDP-43 RNA-binding capacity through a single acetylation-mimic mutation alters TDP-43 function and recapitulates biochemical, molecular, and behavioral features of sporadic TDP-43 proteinopathies, thus providing opportunities for new research into pathogenic mechanisms and therapeutic interventions.

In a mouse model of neurofibromatosis type 1, the purinergic receptor P2RY14 is a key regulator of Schwann cell precursor self-renewal and proliferation, of neurofibroma tumor initiation and of mouse survival.

Maternal loss of imprinting at the Igf2/H19 locus reduces expression of H19 lncRNA and thereby leads to progressive cardiac pathologies in a mouse Beckwith–Wiedemann syndrome model.

H-ABC leukodystrophy results in neurologic decline, hypomyelination and atrophy of the striatum and cerebellum and Tubb4a^D249N/D249Nmouse model recapitulates features of H-ABC disease, providing an important tool for therapeutic development.

Optogenetic and electrical low-frequency stimulation in the sclerotic hippocampus prevents the emergence of spontaneous focal and evoked generalized seizures in a mouse epilepsy model.

A mouse model of Williams–Beuren syndrome allowed us to assess the endocannabinoid system and the impact of targeting the monoacyl glycerol lipase in modulating key phenotypes such as cognitive and hypersocial phenotype as well as the cardiac phenotype.

Auxin-inducible degradation of CRISPR-tagged endogenous proteins in mice reveals cell-type-specific dependence on the mitotic chromosome condensation proteins.