성명 김지은 조교수
학과 생명건강공학과
연구분야 알츠하이머 기전 규명 및 신규 치료제 개발, 퇴행성뇌질환 인지장애 조절 연구
연락처 033-250-6479
이메일 jieunkim@kangwon.ac.kr
학력
2008-2012 부산대학교 생명과학과 생물학 학사
2012-2019 부산대학교 생명시스템학과 뇌신경과학 석·박사
주요경력
2019-2020 한국과학기술연구원(KIST) 신경과학 연구그룹 박사후연구원
2020-2023 한국뇌연구원(KBRI) 퇴행성뇌질환 연구그룹 박사후연구원
2023-현재 강원대학교 의생명과학대학 생명건강공학과 조교수
연구 관심 분야
퇴행성뇌질환 신규 치료제 개발
알츠아이머질병 신경염증, 아밀로이드베타, 타우인산화, 미토콘드리아, 오토파지 및 인지장애 회복 기전 규명
퇴행성뇌질환 발병 유래의 대뇌 보상계 기전 규명
NDST3-induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson’s Disease (2025.11)
Cell lineage transform based AAV gene therapy enables walking again after chronic complete spinal cord injury for preclinical investigation (2025.10)
Glutamine synthetase in astrocytes of the caudate and putamen is responsible for locomotor sensitization after nicotine exposure (2025.09)
Soil nutrient levels determine the factors that influence changes in the soil bacterial community in the Xilingol steppe, inner Mongolia, China (2025.07)
Blockade of forkhead box protein O1 signaling alleviates primary sclerosing cholangitis-induced sarcopenia in mice model (2024.11)
Erlotinib regulates short-term memory, tau/Aβ pathology, and astrogliosis in mouse models of AD (2024.10)
ARNT2 controls prefrontal somatostatin interneurons mediating affective empathy (2024.09)
Comparative analysis of changes in immune cell in the chicken spleen across different ages using flow cytometry (2024.09)
The dopamine analogue CA140 alleviates AD pathology, neuroinflammation, and rescues synaptic/cognitive functions by modulating DRD1 signaling or directly binding to Abeta (2024.08.)
EGFR is a potential dual molecular target for cancer and Alzheimer's disease (2023.08.)
Gene Therapy Using Efficient Direct Lineage Reprogramming Technology for Neurological Diseases (2023.05.)
Genetic deletion of nitric oxide synthase 2 ameliorates Parkinson's disease pathology and neuroinflammation in a transgenic mouse model of synucleinopathy (2023.01.)
Mesoscopic Mapping of Visual Pathway in a Female 5XFAD Mouse Model of Alzheimer's Disease (2022.12.)
L-Type Ca2+ Channel Inhibition Rescues the LPS-Induced Neuroinflammatory Response and Impairments in Spatial Memory and Dendritic Spine Formation (2022.11.)
Inhibiting EGFR/HER-2 ameliorates neuroinflammatory responses and the early stage of tau pathology through DYRK1A (2022.10.)
Nitric Oxide Linked to mGluR5 Upregulates BDNF Synthesis by Activating MMP2 in the Caudate and Putamen after Challenge Exposure to Nicotine in Rats (2022.09.)
Nilotinib modulates LPS-induced cognitive impairment and neuroinflammatory responses by regulating P38/STAT3 signaling (2022.07.)
Donepezil Regulates LPS and A beta-Stimulated Neuroinflammation through MAPK/NLRP3 Inflammasome/STAT3 Signaling (2021.10.)
The Anti-diabetic Drug Gliquidone Modulates Lipopolysaccharide-Mediated Microglial Neuroinflammatory Responses by Inhibiting the NLRP3 Inflammasome (2021.10.)
Emerging pathogenic role of peripheral blood factors following BBB disruption in neurodegenerative disease (2021.07.)
Sorafenib Modulates the LPS- and A beta-Induced Neuroinflammatory Response in Cells, Wild-Type Mice, and 5xFAD Mice (2021.05.)
Ibrutinib modulates A beta/tau pathology, neuroinflammation, and cognitive function in mouse models of Alzheimer's disease (2021.03.)
Repeated nicotine exposure increases the intracellular interaction between ERK-mGluR5 in the nucleus accumbens more in adult than adolescent rats (2021.03.)
Exposure to Commercial Cigarette Smoke Produces Psychomotor Sensitization via Hyperstimulation of Glutamate Response in the Dorsal Striatum (2021.01.)
Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration (2019.06.)