Chang-Hwan Park

TL;DR: An in vitro differentiation protocol to derive an enriched population of midbrain DA neurons from hES cells is reported, and hES cell‐derived DA neurons demonstrated functionality in vitro, releasing DA in response to KCl‐induced depolarization and reuptake of DA.

TL;DR: The clinical potential of protein-based hiPSCs for personalized cell therapy of PD is supported and transplantation of these cells into rats with striatal lesions, a model of PD, significantly rescued motor deficits.

TL;DR: Deep hybrid capture and amplicon sequencing of five important mTOR pathway genes shows that brain somatic mutations in TSC1 and TSC2 cause FCD and that in utero application of the CRISPR-Cas9 system is useful for generating neurodevelopmental disease models of somatic mutation in the brain.

TL;DR: It is found that two antimalarial drugs, amodiaquine and chloroquine stimulate the transcriptional function of Nurr1 through physical interaction with its ligand binding domain (LBD), offering proof of principle that small molecules targeting the Nurr 1 LBD can be used as a mechanism-based and neuroprotective strategy for PD.

TL;DR: Foxa2, a forkhead transcription factor whose role in midbrain DA neuron development was recently revealed, synergistically cooperates with Nurr1 to induce DA phenotype acquisition, midbrain‐specific gene expression, and neuronal maturation and these findings can be applied to ongoing attempts to develop an efficient and safe precursor/stem cell‐based therapy for Parkinson's disease.