신정환 교수
Jung Hwan Shin
서울대학교 · 의학
연구실 소개
신정환 교수의 연구실은 뇌의 기능적 회로, 특히 편두통성 어지러움과 파킨슨병 등 신경퇴행성질환의 신경기전을 해부하고자 합니다. 주로 뇌간-시상-皮질 경로의 기능적 활성화와 기저구애의 직접/간접 경로 신경세포의 상호작용을 동물 모델과 영상기술을 통해 규명하며, 보상 기반 학습과 운동 조절의 뇌 기반 메커니즘을 밝혀내고자 합니다. 또한, 알파-시누클레인과 타우 단백질의 세포 간 전파 및 신경염증 반응을 중심으로 신경퇴행성질환의 질병 수정 치료 전략을 모색하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15During the attacks of vestibular migraine, the increased metabolism in the temporo-parieto-insular areas and bilateral thalami indicates activation of the vestibulo-thalamo-cortical pathway, and decreased metabolism in the occipital cortex may represent reciprocal inhibition between the visual and vestibular systems.
The direct and indirect pathways of the basal ganglia have long been thought to mediate behavioral promotion and inhibition, respectively. However, this classic dichotomous model has been recently challenged. To better understand neural processes underlying reward-based learning and movement control, we recorded from direct (dSPNs) and indirect (iSPNs) pathway spiny projection neurons in the dorsomedial striatum of D1-Cre and D2-Cre mice performing a probabilistic Pavlovian conditioning task. dS
To obtain insights into striatal neural processes underlying reward-based learning and movement control, we examined spatial organizations of striatal neurons related to movement and reward-based learning. For this, we recorded the activity of direct- and indirect-pathway neurons (D1 and A2a receptor-expressing neurons, respectively) in mice engaged in probabilistic classical conditioning and open-field free exploration. We found broadly organized functional clusters of striatal neurons in the d
Baseline and longitudinal monitoring of the DAT pattern can be a useful biomarker in identifying individuals with a high risk of disease conversion and in selecting the potential population for clinical trials in iRBD.
This study provides Class IV evidence that a de novo PD pattern on FDG-PET predicts future conversion to neurodegenerative disease in patients with iRBD.
α-Synuclein and tau deposition in the central nervous system is responsible for various parkinsonian syndromes, including Parkinson's disease, multiple system atrophy, dementia with Lewy bodies, progressive supranuclear palsy and corticobasal degeneration. Emerging evidence has suggested that pathologic α-synuclein and tau are transmitted from cell to cell and further accelerate the aggregation of pathologic proteins in neighboring cells. Furthermore, extracellular pathologic proteins have also
Because the statistical analysis between the normal controls and patients with low range expansions failed to show any differences so far, we must consider that clinical cases with low range expansions could be idiopathic movement disorders showing coincidental CAG/CAA expansions. Thus, we need to reconsider the pathologic role of low range expansions (41-42). Long term follow up and comprehensive investigations using autopsy and imaging studies in patients and controls with low range expansions
Cortical thickness signature can effectively reflect the longitudinal evolution of Lewy body dementia in the iRBD population. Replication studies would further validate the utility of this imaging marker in iRBD.
To elucidate the biomarkers related to survival in multiple system atrophy(MSA), we analyzed the predictability of retrospectively collected blood markers for survival in 650 probable MSA. High absolute neutrophil count, red-cell distribution width, C-reactive protein, erythrocyte sedimentation rate, and low hemoglobin, protein, albumin, and creatinine were correlated with higher mortality in MSA. Systemic alteration in inflammation and nutritional status in the early stage are associated with h
The deep learning-based pose-estimation algorithm objectively measured postural abnormalities in PD patients.
No significant differences were found in the effects of the preservative-free fourth-generation fluoroquinolones gatifloxacin and moxifloxacin on epithelial healing after PRK.
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