Parkinson's Disease Mechanisms and Treatments

The paper re-evaluates TMEM230 mutations in familial Parkinson’s disease using updated genetic data and experiments, confirming TMEM230 as a PD-causing gene.

The paper identifies β-synuclein on secretory granules in chromaffin cells and shows that α-synuclein accelerates BDNF discharge by speeding fusion pore expansion.

This study examines the distribution of α-synuclein pathology in insular cortex sub-regions in Parkinson’s disease and dementia with Lewy bodies, revealing regional differences in vulnerability.

This study compares mRNA-Seq data from Huntington and Parkinson Diseases to identify common and unique transcriptional signatures, revealing shared inflammatory processes and differential biological pathway enrichments.

This study transplants Parkinson's patient iPSC-derived neurons into mice, finding increased alpha-Synuclein levels but no spreading in the mouse brain.

The paper examines how Parkinson’s disease and aging affect cognitive performance in rehabilitation volunteers, finding that PD volunteers often outperform neurotypical volunteers after controlling for age.

The paper refutes the claim that TMEM230 c.422G>T is a causative mutation for Parkinson disease by showing it is not present in affected family members.