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In-Hee Mok

Seoul National University · 医学

研究室紹介

Professor In-Hee Mok's research lab focuses on the molecular and cellular mechanisms underlying Alzheimer's disease (AD), with a particular emphasis on amyloid-beta (Aβ) metabolism, tau pathology, and mitochondrial dysfunction. The lab investigates the role of glial cells—especially microglia—in Aβ plaque formation and neuroinflammation, as well as the potential of natural compounds like ginsenosides and asiaticoside derivatives in neuroprotection. Using in vivo models, PET imaging, and biochemical approaches, the lab explores biomarkers such as plasma tau and Aβ, aiming to bridge peripheral markers with central nervous system pathology. Their work also delves into unconventional protein secretion, particularly of insulin-degrading enzyme (IDE), which plays a key role in Aβ degradation.

Alzheimer's diseaseamyloid-betatau pathologymicroglianeuroprotection

Research Overview

Papers
294
Total Citations
15,548
Papers (5y)
45
Primary Field
医学

Research Output Trend

Figures are computed from collected data and may differ slightly.

Publications per year (5y)
45total
2022
2023
2024
2025
2026
Citations per year (5y)
661total
20222023202420252026

Selected Papers

15
1
Article|835 citations·2019
A Breakdown in Metabolic Reprogramming Causes Microglia Dysfunction in Alzheimer's Disease
Sung-Hoon Baik, Seokjo Kang, Woochan Lee, Hayoung Choi, Sunwoo Chung, Jong‐Il Kim, Inhee Mook‐Jung
SJR Q1Cell MetabolismOA
NeurologyNeuroscience
2
Article|659 citations·2016
Mitochondria-Targeting Ceria Nanoparticles as Antioxidants for Alzheimer’s Disease
Hyek Jin Kwon, Moon-Yong Cha, Dokyoon Kim, Dong‐Kyu Kim, Min Soh, Kwangsoo Shin, Taeghwan Hyeon, Inhee Mook‐Jung
SJR Q1ACS Nano

Mitochondrial oxidative stress is a key pathologic factor in neurodegenerative diseases, including Alzheimer's disease. Abnormal generation of reactive oxygen species (ROS), resulting from mitochondrial dysfunction, can lead to neuronal cell death. Ceria (CeO2) nanoparticles are known to function as strong and recyclable ROS scavengers by shuttling between Ce(3+) and Ce(4+) oxidation states. Consequently, targeting ceria nanoparticles selectively to mitochondria might be a promising therapeutic

Materials ChemistryMaterials Science
3
Article|230 citations·2016
Microglia contributes to plaque growth by cell death due to uptake of amyloid β in the brain of Alzheimer's disease mouse model
Sung-Hoon Baik, Seokjo Kang, Sung Min Son, Inhee Mook‐Jung
SJR Q1Glia

Pathological hallmarks of Alzheimer's disease (AD) include extracellularly accumulated amyloid β (Aβ) plaques and intracellular neurofibrillary tangles in the brain. Activated microglia, brain-resident macrophages, are also found surrounding Aβ plaques. The study of the brain of AD mouse models revealed that Aβ plaque formation is completed by the consolidation of newly generated plaque clusters in vicinity of existed plaques. However, the dynamics of Aβ plaque formation, growth and the mechanis

NeurologyNeuroscience
4
Article|229 citations·2012
Mitochondria-Specific Accumulation of Amyloid β Induces Mitochondrial Dysfunction Leading to Apoptotic Cell Death
Moon-Yong Cha, Sun-Ho Han, Sung Min Son, Hyun-Seok Hong, Young-Ju Choi, Jayoung Byun, Inhee Mook‐Jung
SJR Q1PLoS ONEOA

Mitochondria are best known as the essential intracellular organelles that host the homeostasis required for cellular survival, but they also have relevance in diverse disease-related conditions, including Alzheimer's disease (AD). Amyloid β (Aβ) peptide is the key molecule in AD pathogenesis, and has been highlighted in the implication of mitochondrial abnormality during the disease progress. Neuronal exposure to Aβ impairs mitochondrial dynamics and function. Furthermore, mitochondrial Aβ accu

PhysiologyMedicine
5
Article|218 citations·2021
A logical network-based drug-screening platform for Alzheimer’s disease representing pathological features of human brain organoids
Jong‐Chan Park, So‐Yeong Jang, Dongjoon Lee, Jeong-Ha Lee, Uiryong Kang, Hongjun Chang, Haeng Jun Kim, Sun-Ho Han, Jinsoo Seo, Murim Choi, Dong Young Lee, Min Soo Byun
SJR Q1Nature CommunicationsOA

Developing effective drugs for Alzheimer's disease (AD), the most common cause of dementia, has been difficult because of complicated pathogenesis. Here, we report an efficient, network-based drug-screening platform developed by integrating mathematical modeling and the pathological features of AD with human iPSC-derived cerebral organoids (iCOs), including CRISPR-Cas9-edited isogenic lines. We use 1300 organoids from 11 participants to build a high-content screening (HCS) system and test blood-

Molecular BiologyBiochemistry, Genetics and Molecular Biology
6
Article|200 citations·2015
Two-Photon Absorbing Dyes with Minimal Autofluorescence in Tissue Imaging: Application toin VivoImaging of Amyloid-β Plaques with a Negligible Background Signal
Dokyoung Kim, Hyunsoo Moon, Sung-Hoon Baik, Subhankar Singha, Yong Woong Jun, Taejun Wang, Ki Hean Kim, Byung Sun Park, Junyang Jung, Inhee Mook‐Jung, Kyo Han Ahn
SJR Q1Journal of the American Chemical Society

Fluorescence imaging of tissues offer an essential means for studying biological systems. Autofluorescence becomes a serious issue in tissue imaging under excitation at UV-vis wavelengths where biological molecules compete with the fluorophore. To address this critical issue, a novel class of fluorophores that can be excited at ∼900 nm under two-photon excitation conditions and emits in the red wavelength region (≥600 nm) has been disclosed. The new π-extended dipolar dye system shows several ad

BiophysicsBiochemistry, Genetics and Molecular Biology
7
Article|190 citations·2018
Plasma tau/amyloid-β1–42 ratio predicts brain tau deposition and neurodegeneration in Alzheimer’s disease
Jong‐Chan Park, Sun-Ho Han, Dahyun Yi, Min Soo Byun, Jun Ho Lee, Sukjin Jang, Kang Ko, So Yeon Jeon, Yun‐Sang Lee, Yu Kyeong Kim, Dong Young Lee, Inhee Mook‐Jung
SJR Q1BrainOA

One of the hallmarks of Alzheimer's disease is abnormal deposition of tau proteins in the brain. Although plasma tau has been proposed as a potential biomarker for Alzheimer's disease, a direct link to brain deposition of tau is limited. Here, we estimated the amount of in vivo tau deposition in the brain by PET imaging and measured plasma levels of total tau (t-tau), phosphorylated tau (p-tau, T181) and amyloid-β1-42. We found significant correlations of plasma p-tau, t-tau, p-tau/amyloid-β1-42

PhysiologyMedicine
8
Article|175 citations·2014
Migration of neutrophils targeting amyloid plaques in Alzheimer's disease mouse model
Sung-Hoon Baik, Moon-Yong Cha, Young‐Min Hyun, Hansang Cho, Bashar Hamza, Dong‐Kyu Kim, Sun-Ho Han, Hee-Sun Choi, Kyung Ho Kim, Minho Moon, Jeewoo Lee, Minsoo Kim
SJR Q1Neurobiology of AgingOA
PhysiologyMedicine
9
Article|164 citations·2005
Amyloid peptide attenuates the proteasome activity in neuronal cells
Sang-Soo Oh, Hyun Seok Hong, Enmi Hwang, Hae Jin Sim, Woojin Lee, Su Jeon Shin, Inhee Mook‐Jung
SJR Q1Mechanisms of Ageing and Development
Molecular BiologyBiochemistry, Genetics and Molecular Biology
10
Article|154 citations·2015
Aβ-induced degradation of BMAL1 and CBP leads to circadian rhythm disruption in Alzheimer’s disease
Hyundong Song, Minho Moon, Han Kyoung Choe, Dong-Hee Han, Changhwan Jang, Ahbin Kim, Sehyung Cho, Kyungjin Kim, Inhee Mook‐Jung
SJR Q1Molecular NeurodegenerationOA

BACKGROUND: Patients with Alzheimer's disease (AD) frequently experience disruption of their circadian rhythms, but whether and how circadian clock molecules are perturbed by AD remains unknown. AD is an age-related neurological disorder and amyloid-β (Aβ) is one of major causative molecules in the pathogenesis of AD. RESULTS: In this study, we investigated the role of Aβ in the regulation of clock molecules and circadian rhythm using an AD mouse model. These mice exhibited altered circadian beh

Endocrine and Autonomic SystemsNeuroscience
11
Article|145 citations·2001
Ginsenoside Rb1 and Rg1 improve spatial learning and increase hippocampal synaptophysin level in mice
Inhee Mook‐Jung, Hyun‐Seok Hong, Jung Hyun Boo, Kang Hee Lee, Sung Hwan Yun, Mi Young Cheong, In-Soo Joo, Kyoon Huh, Min Whan Jung
SJR Q2Journal of Neuroscience Research

We investigated the cognition enhancing effects of ginsenoside Rb1 and Rg1. Mice were trained in a Morris water maze following injection (i.p.) of Rb1 (1 mg/kg) or Rg1 (1 mg/kg) for 4 days. Both Rb1- and Rg1-injected mice showed enhanced spatial learning compared to control animals. The hippocampus, but not the frontal cortex, of treated mice contained higher density of a synaptic marker protein, synaptophysin, compared to control mice. Electrophysiological recordings in hippocampal slices revea

Cellular and Molecular NeuroscienceNeuroscience
12
Article|137 citations·1999
Protective effects of asiaticoside derivatives against beta-amyloid neurotoxicity
Inhee Mook‐Jung, Jieun Shin, Sung Hwan Yun, Kyoon Huh, Jae Young Koh, Hyung Keun Park, Sang‐sup Jew, Min Whan Jung
SJR Q2Journal of Neuroscience ResearchOA

Asiaticoside (AS) derivatives were tested for potential protective effects against Abeta-induced cell death. Of the 28 AS derivatives tested, asiatic acid (AA), asiaticoside 6 (AS6), and SM2 showed strong inhibition of Abeta-induced death of B103 cells at 1 microM. The three AS derivatives were further tested for their effects on free radical injury and apoptosis. All three AS derivatives reduced H(2)O(2)-induced cell death and lowered intracellular free radical concentration, but AA showed the

Complementary and alternative medicineMedicine
13
Article|135 citations·2011
Aβ-induced formation of autophagosomes is mediated by RAGE-CaMKKβ-AMPK signaling
Sung Min Son, Eun Sun Jung, Hong Joon Shin, Jayoung Byun, Inhee Mook‐Jung
SJR Q1Neurobiology of Aging
Clinical BiochemistryBiochemistry, Genetics and Molecular Biology
14
Article|130 citations·2016
Insulin-degrading enzyme secretion from astrocytes is mediated by an autophagy-based unconventional secretory pathway in Alzheimer disease
Sung Min Son, Moon-Yong Cha, Hee-Sun Choi, Seokjo Kang, Hyunjung Choi, Myung‐Shik Lee, Sun Ah Park, Inhee Mook‐Jung
SJR Q1AutophagyOA

The secretion of proteins that lack a signal sequence to the extracellular milieu is regulated by their transition through the unconventional secretory pathway. IDE (insulin-degrading enzyme) is one of the major proteases of amyloid beta peptide (Aβ), a presumed causative molecule in Alzheimer disease (AD) pathogenesis. IDE acts in the extracellular space despite having no signal sequence, but the underlying mechanism of IDE secretion extracellularly is still unknown. In this study, we found tha

PhysiologyMedicine
15
Article|125 citations·2002
Lovastatin enhances Aβ production and senile plaque deposition in female Tg2576 mice
In-Ho Park, Eun Mi Hwang, Hyun Seok Hong, Jung Hyun Boo, Sang Soo Oh, Jeewoo Lee, Min Whan Jung, Oh Young Bang, Seung Up Kim, Inhee Mook‐Jung
SJR Q1Neurobiology of Aging
PhysiologyMedicine

Research Areas

PhysiologyMolecular BiologyNeurologySpectroscopyCellular and Molecular NeuroscienceClinical Biochemistry

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