Mark S. Moehle

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

This study investigates the potential of M5 positive allosteric modulators to alleviate parkinsonian motor deficits without causing dyskinesia or impairing L-DOPA efficacy.

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.

The paper shows that inhibiting LRRK2 kinase activity rescues dopamine deficits in VPS35 p.D620N knock-in mice by normalizing DAT function and reducing hyperlocomotion.

This study tests whether selective modulation of muscarinic receptors M1, M4, or M5 can reduce parkinsonian tremor, finding no effect and suggesting M2 or M3 receptors may be responsible for anti-tremor efficacy.