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

The promising potential of plasma extracellular vesicle synaptic proteins as clinical biomarkers of disease progression in Parkinson's disease has been presented.

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 hypo- versus hyperkinetic nature of Parkinson’s disease and dystonia, respectively, may be reflected by differences in disease-specific spiketrain dynamics and striato-pallidal synaptic plasticity.

Downregulation of PTBP1 in neurons, but not astrocytes, alleviates motor symptoms in a Parkinson’s disease mouse model by inducing dopaminergic marker expression in striatal neurons and increasing striatal dopamine levels.

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.