Seoul National University · 医学
Professor Jee-Young Lee's research lab focuses on the genetic, neurobiological, and neuroimaging mechanisms underlying non-motor and motor complications in Parkinson’s disease. Key research directions include identifying genetic susceptibility variants—particularly in dopamine, glutamate, and serotonin-related genes—that contribute to impulse control behaviors, levodopa-induced dyskinesias, and visual hallucinations. The lab integrates clinical genetics, neuroimaging (e.g., optical coherence tomography), and molecular biology to explore the structural and functional basis of visual and neuropsychiatric symptoms in PD. Their work also investigates tumor suppressor pathways involving TTP and let-7 microRNA in cancer, highlighting a translational interest in gene regulation and neurodegeneration.
Figures are computed from collected data and may differ slightly.
We aimed to assess whether allelic variants of dopamine receptor, glutamate receptor, and serotonin transporter genes are associated with the appearance of impulse control and related behaviors (ICRB) in Parkinson's disease (PD) with dopamine replacement therapy (DRT). We surveyed ICRB in consecutive Korean patients with PD who were treated with stable DRT using modified Minnesota Impulsive Disorders Interview over a period of 4 months. In the 404 patients who completed the interview and the 559
Defective visual information processing from both central and peripheral pathways is one of the suggested mechanisms of visual hallucination in Parkinson's disease (PD). To investigate the role of retinal thinning for visual hallucination in PD, we conducted a case-control study using spectral domain optical coherence tomography. We examined a representative sample of 61 patients with PD and 30 healthy controls who had no history of ophthalmic diseases. General ophthalmologic examinations and op
To examine whether there is a differential genetic susceptibility in the diphasic and peak-dose forms of levodopa-induced dyskinesias (LID) in patients with Parkinson's disease (PD). The study cohort comprised 503 unrelated Korean PD patients who were treated with levodopa and had a disease duration of at least 5 years. The presence of LID was identified during a routine follow-up and special care was taken to separate the two distinct forms of LID into diphasic and peak-dose dyskinesias (PDSK).
Visual symptoms are a common feature in patients with Parkinson's disease (PD), and retinal dopamine loss and dysfunctions in foveal vision have been described in PD patients. Because visual hallucination (VH) is a specific feature of PD which is differentiated from other parkinsonian disorders, defective visual information processing from both the central and peripheral pathways is suggested to be the pathophysiological mechanisms of VH in PD. Decreased visual acuity as well as impaired contras
Tristetraprolin (TTP) and let-7 microRNA exhibit suppressive effects on cell growth through down-regulation of oncogenes. Both TTP and let-7 are often repressed in human cancers, thereby promoting oncogenesis by derepressing their target genes. However, the precise mechanism of this repression is unknown. We here demonstrate that p53 stimulated by the DNA-damaging agent doxorubicin (DOX) induced the expression of TTP in cancer cells. TTP in turn increased let-7 levels through down-regulation of
Relative serotonergic innervation of the putamen and pallidum increased with clinical PD progression and was highest in patients with established dyskinesia. The serotonin/dopamine transporter ratio might be a potential marker of disease progression and an indicator of risk for levodopa-induced dyskinesia in PD. A prospective evaluation is warranted in the future.
A great gap in extrastriatal versus striatal dopaminergic fibre degenerations is an intrinsic condition predisposing to ICD in PD. Distinct pattern of extrastriatal changes between the ICD and non-ICD patients could provide a further insight into a mechanism of ICD in PD.
Macular ganglion cell complex thinning may be a marker of neurodegeneration in prodromal Parkinson's disease. © 2019 International Parkinson and Movement Disorder Society.
The diagnosis of multiple system atrophy (MSA) is mainly based on the clinical criteria, which are often of little assistance in the early stages of the disease. Positional downbeat nystagmus (pDBN) and perverted head-shaking nystagmus (pHSN), possible signs of cerebellar dysfunction, may be useful in differentiating MSA from other parkinsonian disorders. To investigate the occurrences of pDBN and pHSN in patients with MSA compared with those in patients with Parkinson's disease (PD). A total of
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