The pattern of atrophy in Parkinson's disease is consistent with the disease spreading via intrinsic brain networks.

Extracellular vesicles are proposed as novel, non-cell-autonomous mediators of neuronal atrophy in Parkinson's disease.

In contrast to previous post-mortem or fixed tissue histochemical reports, live calcium and mitochondrial imaging data suggest that the enteric nervous system is not generally affected in Parkinson's disease patients.

The structure of human PINK1 explains structural regulation and clarity on the impact of loss of function disease-associated mutations, which may stimulate future drug discovery efforts for both familial and idiopathic Parkinson's disease.

Regulation of Cav2.3 Ca²⁺ channels by membrane-bound β2 subunit splice variants permits long-lasting channel activity even during prolonged and continuous activity in dopamine neurons, with implications for Parkinson's disease pathophysiology.

Motor signs of Parkinson’s disease such as tremor and bradykinesia are independently expressed and exhibit distinct signatures of neural activity that can independently decoded from subthalamic and cortical recordings using interpretable machine learning.

High-frequency stimulation of the upper thoracic spinal cord corrects anticipatory postural adjustments and improving gait efficiency and inhibiting freezing of gait episodes in advanced Parkinson's disease.

Patients with DYT1 dystonia show aberrant risk-aversion in a simple decision-making task, in accordance with predictions of a reinforcement learning model of corticostriatal trial-and-error learning.

Long studied in the context of the central nervous system, LRRK2 also functions in peripheral immunity by maintaining mitochondrial homeostasis in macrophages to regulate the type I interferon response.

By reducing mitochondrial fusion, MUL1 compensates for the mutations in PINK1 or parkin that underlie certain cases of Parkinson's disease.