Bradykinesia in Parkinson's disease may be associated to a dopamine-dependent recruitment failure of subthalamic activity in short bursts of gamma synchrony.
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.
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.
A crucial step during the mitophagy cascade involves the disassembly of connections between mitochondria and the endoplasmic reticulum via the retrotranslocation of Mfn2 tethering complexes by the Parkinson's disease genes PARKIN and PINK1, as well as the ATPase VCP/p97.
