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.

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

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.

Ataxin-2 interacts with neuronal mRNA in RNP granules.

Covert visual attention modulates alpha-band traveling waves propagating from frontal to occipital regions in both hemispheres, yet it modulates waves propagating in the opposite direction (occipital to frontal) only in the presence of visual stimulation.

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.

Psychedelics induce a pattern of cortical activity very similar to the one observed during visual perception, despite participants had shut eyes.

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.

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.