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서울대학교 뇌과학 협동과정

Interdisciplinary
Program in
Neuroscience

두뇌 및 신경계를 탐구하는 서울대학교 뇌과학협동과정

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교수진

이승재 Ph.D.

교수
| 의과대학 의과학과

 

sjlee66@snu.ac.kr

전화번호:
(82)2-3668-7037 (Lab)

서울특별시 종로구 대학로 103
서울대학교 의과대학
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연구분야

Neurological Disorder

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자연과학대학 뇌과학협동과정

  • Research Overview

    신경질환 실험실 (Laboratory of Neurological Disease)

    The major interests of my group include the topics, such as the mechanism of disease progression, determinants for disease specificity (eg, Alzheimer vs. Parkinson), and mechanism-based development of diagnosis and therapy. Specific questions to address are the followings.

    -What is the underlying mechanism for the ‘progression’ of neurodegenerative diseases?
    -Which aggregate species are pathogenic culprit?
    -What is the relationship between lysosomal storage diseases and neurodegenerative diseases?
    -Why does some people get tauopathies, while others get synucleinopathies or TDP43pathies?
    -Can we stop the progression of neurodegenerative diseases by interfering with protein aggregate spreading?


    이러한 문제들을 해결하기 위하여 신경질환 실험실에서는 다양한 접근 방법을 활용하고 있습니다. (1) 신경세포 및 교세포들을 배양하여 이들을 형광이미징과 생화학적인 기법을 사용하여 분석하며, (2) 유전자 조작 마우스 모델과 예쁜꼬마선충 모델을 사용하여 질환의 병리적/행동학적 형질을 분석하며, (3) 단세포 전사체 분석 등을 활용하여 생물정보학적 분석을 수행하고 있습니다.

    또한, 신경질환 실험실에서는 바이오텍 회사와의 협업을 통하여 파킨슨병, 다계통 위측증 등 퇴행성뇌질환의 진행을 억제하는 disease-modifying drug 개발을 추진하고 있습니다. 특히, 개발 중인 신약 후보의 작용 기전 연구 및 신규 치료 타겟의 동정에 많은 노력을 기울이고 있습니다.
  • 연구성과

    2021

    Wulansari N, Darsono WHW, Woo HJ, Chang MY, Kim J, Bae EJ, Sun W, Lee JH, Cho IJ, Shin H, Lee SJ*, Lee SH*. Neurodevelopmental defects and neurodegenerative phenotypes in human brain organoids carrying Parkinson's disease-linked DNAJC6 mutations. Sci Adv. 2021 doi: 10.1126/sciadv.abb1540. (*co-corresponding authors)

    2019

    Timo Strohäker, Byung Chul Jung, Shu-Hao Liou, Claudio O. Fernandez, Dietmar Riedel, Stefan Becker, Glenda M. Halliday, Marina Bennati, Woojin S. Kim*,Seung-Jae Lee*, and Markus Zweckstetter*. Structural heterogeneity of α-synuclein fibrils amplified from patient brain extracts. Nat Commun. 2019;10(1):5535. doi: 10.1038/s41467-019-13564-w. (*co-corresponding authors)

    2019

    Jun Sung Lee, Kazuaki Kanai, Mari Suzuki, Woojin S. Kim, Han Soo Yoo, YuHong Fu, Dong-Kyu Kim, Byung Chul Jung, Minsun Choi, Kyu Won Oh, Yuanzhe Li, Mitsuyoshi Nakatani, Tomoko Nakazato, Satoko Sekimoto, Manabu Funayama, Hiroyo Yoshino, Shin-ichiro Kubo, Kenya Nishioka, Ryusuke Sakai, Morio Ueyama, Hideki Mochizuki, He-Jin Lee, Sergio Pablo Sardi, Glenda M. Halliday, Yoshitaka Nagai, Phil Hyu Lee, Nobutaka Hattori and Seung-Jae Lee. Arylsulfatase A, a genetic modifier of Parkinson’s disease, is an a-synuclein chaperone. BRAIN. 2019, doi: 10.1093/brain/awz205

    2018

    Bae E-J, Kim D-K, Kim C, Mante M, Adame A, Rockenstein E, Ulusoy A, Klinkenberg M, Jeong GR, Bae JR, Lee C, Lee H-J, Lee B-D, Di Monte DA, Masliah E, Lee S-J. LRRK2 kinase regulates -synuclein propagation via RAB35 phosphorylation. Nature Commun, 9(1):3465. doi: 10.1038/s41467-018-05958-z

    2018

    Lim S, Kim H-J, Kim D-K, Lee S-J. Non-cell-autonomous actions of alpha-synuclein: implications in glial synucleinopathies. Prog Neurobiol, 2018, 169, 158-171

    2016

    Kim DK, Lim HS, Kawasaki I, Shim YH, Vaikath NN, El-Agnaf OMA, Lee HJ, Lee S-J. Anti-aging treatments slow propagation of synucleinopathy by restoring lysosomal function. Autophagy, 2016, 12, 1849-1863

    2015

    Kim C, Rockenstein E, Spencer B, Kim H-K, Adame A, Trejo M, Stafa K, Lee H-J, Lee S-J,*, Masliah E,* (2015) Antagonizing neuronal Toll-like receptor 2 prevents synucleinopathy by activating autophagy. Cell Reports, 13, 771-782 *Co-corresponding authors

    2015

    Lee S-J, Masliah E (2015) Aggregates feel the strain. Nature, 522, 296-297

    2014

    Bae E-J, Yang N-Y, Song M, Lee CS, Lee H-J, Masliah E, Sardi SP, Lee S-J (2014) Glucocerebrosidase deficiency enhances cell-to-cell transmission of -synuclein. Nature Communications, 5:4755 doi: 10.1038/ncomms5755

    2014

    Lee H-J, Bae E-J, Lee S-J. (2014) Extracelullar a-synuclein: A novel and crucial factor in Lewy body diseases. Nature Rev. Neurol., doi:10.1038/nrneurol.2013.275

    2013

    Kim C, Ho D-H, Suk J-E, You S, Michael S, Kang J, Lee S, Masliah E, Hwang D, Lee H-J, Lee S-J (2013) Neuron-released oligomeric α-synuclein is an endogenous agonist of TLR2 for paracrine activation of microglia. Nature Commun. 4:1562 | DOI: 10.1038/ncomms2534

    2010

    Lee S-J, Desplats P, Sigurdson C, Tsigelny I, Masliah E (2010) Cell-Cell Transmission of Non-Prion Protein Aggregates, Nature Review Neurology, 6, 702-706

    2009

    Desplats P*, Lee H-J*, Bae E-J, Patrick C, Rockenstein E, Crews L, Spencer B, Masliah E, Lee S-J (2009) Inclusion formation and neuronal cell death through neuron-to-neuron transmission of alpha-synuclein. Proc. Nat. Acad. Sci. USA, 106, 13010-13015 (* equal contribution) Cover highlight


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