Dr. Kim’s research focuses mainly on the elucidation of the molecular mechanisms underlying oxidative stress-related nigrostriatal degeneration in Parkinson’s disease (PD) using postmortem brain samples and a range of rodent PD models. He reported for the first time that NADPH oxidase 1 (NOX1) is expressed in dopaminergic neurons and that NOX1-derived ROS is responsible for dopaminergic neuronal degeneration and α-synuclein aggregation, which are pathological hallmarks of PD. Currently, his research is expanding to investigate the molecular mechanisms governing oxidative stress-mediated α-synuclein changes including epigenetic and translational regulation as well as protein aggregation and impact on mitochondrial functions. He has recently introduced the innovative concept of transcriptional mutagenesis of the SNCA gene and its contribution to PD pathogenesis. This original idea is widely applicable to other neurodegenerative conditions including Dementia with Lewy Bodies (DLB) and Alzheimer’s disease. Recently his lab has pioneered PD postmortem brain study by employing multiomic approach of combined single-nuclei RNA- and ATAC-seq. This innovative approach opens a new avenue for our understanding of cell-type specific transcriptional as well as epigenetic mechanisms underpinning PD pathogenesis. His research pipeline is highly interdisciplinary and integrates core areas of neurodegenerative diseases.