Ataxin-2 interacts with neuronal mRNA in RNP granules.

A genetic mutation that impairs autophagic flux leads to neurodegeneration and can cause ataxia and developmental delay in children.

A damaging form of positive feedback linking elevated calcium levels and metabotropic glutamate receptor function in Purkinje neurons plays a critical role in the pathology in spinocerebellar ataxias.

An unbiased biochemical screen reveals a direct link between gene regulation and actin cytoskeleton remodeling.

Restoration of endogenous frataxin levels reverses neurologic and cardiac phenotypes associated with Friedreich's ataxia in adult mice even after significant motor dysfunction.

Ataxia, dystonia, and tremor phenotypes have distinct and generalizable cerebellar interposed nucleus spike signatures in mice, with defining features identified using a classifier model and pathogenicity tested using optogenetic manipulations.

LocoMouse analysis of severely ataxic reeler mutant mice reveals fundamental features of locomotor ataxia and provides a roadmap for linking high-dimensional behavioral phenotyping to alterations in underlying neural circuits.

Progressive changes in Purkinje neuron perturbations and overall cerebellar atrophy correlate for the first time with the development of an overt loss of motor function in a novel mouse model of Ataxia Telangiectasia.

Studies in a mouse model of spinocerebellar ataxia type 1 show that a protein called capicua stabilizes toxic ataxin-1 oligomers offering a possible explanation for regional patterns of neurodegeneration.

Analysis of 3D paw kinematics and whole-body coordination in freely walking mice isolates specific features of gait ataxia and supports the hypothesis that the cerebellum provides an internal forward model for motor control.