Bradykinesia in Parkinson's disease may be associated to a dopamine-dependent recruitment failure of subthalamic activity in short bursts of gamma synchrony.
Pathogenic LRRK2kinase requires Rab10 and RILPL1 to block primary cilia formation, shortening cilia on cholinergic neurons needed for a hedgehog driven circuit that supports dopaminergic neurons in mouse brain.
Memory over 24 hours was impaired in Parkinson's patients off, rather than on, dopaminergic medication during reinforcement learning, whereas dopamine did not affect positive and negative reinforcement, in contrast to previous studies.
Discovery of a physiological LRRK2 substrate and a new mechanism of Rab regulation should aid Parkinson’s research and the understanding of Rab function.
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.
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.
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.
Loss of a developmentally essential gene in adulthood is tolerated in mice, thus offering potential therapeutic options for Alzheimer's and Parkinson's disease.
The spiking activity of the subthalamic nucleus, rather than the activity of striatal projection neurons, orchestrates basal ganglia downstream activity and output commands in health and Parkinson’s disease.
