Michael Millett

This study shows that α-synuclein aggregates in corticostriatal terminals impair glutamatergic transmission without causing neurodegeneration.

This study shows pathological α-synuclein localizes in the nucleus, causing nuclear damage and dysfunction in synucleinopathy models and human tissue.

This study shows that aggregated α-synuclein impairs corticostriatal synaptic function and reduces synaptic density in mice, with some synapses showing increased volume.

Knocking out Gnal in the striatum of mice leads to dystonia-like motor symptoms and increased excitability in striatal spiny projection neurons.

This study characterizes Gnal expression in the mouse brain and shows its role in motor-related neurons through conditional knockout experiments.