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Inhee Mook-Jung has been studied the molecular pathogenesis of Alzheimer's disease (AD). AD is an age-associated neurodegenerative disease and the most common type of dementia. The major pathological hallmarks of AD are extracellularly deposited amyloid plaques and intracellularly accumulated neurofibrillary tangles. Inhee Mook's group has been interested in three big categories. (1) Molecular pathogenesis of AD, including Abeta-tau axis, tau propagation in the brain, brain inflammation including microglial function, gut-brain axis and crosstalk between peripheral and CNS immune system (2) Identification of plasma biomarkers for early diagnosis of dementia (3) Therapeutic approaches for AD drug development such as patient-derived brain organoids and microglia, platform development of drug screening and development of preclinical animal models. Her research contributes to understanding molecular pathophysiology of AD and makes possible to bridge from basic science to clinical application in AD.

Inhee Mook is currently a Professor of College of Medicine at Seoul National University and she is a director of Korea Dementia Research Center since August 2020. She earned her PhD in Cell Biology and Anatomy from the University of Arizona, USA in 1995. Since she has started her own research career at the Ajou University College of Medicine in 1996, she has over 180 refereed publications and 20 patents. She received the Korea Loreal-UNESCO Woman Scientist Award (2015) and Dong Hun Award from Society for Biochemistry and Molecular Biology (2019).

Representative papers
- A breakdown in metabolic reprogramming causes microglia dysfunction in Alzheimer's disease. Cell Metabolism (2019) 30(3):493-507.
- Transfer of a healthy microbiota reduces amyloid and tau pathology in an Alzheimer's disease animal model. Gut (2020) 69(2):283-294.
- Plasma tau/amyloid beta 1-42 ratio predicts brain tau deposition and neurodegeneration in Alzheimer's disease. Brain. (2019) 142(3);771-786.
- Prognostic plasma protein panel for A¥â deposition in the brain in Alzheimer's disease. Prog Neurobiol. (2019) 183:101690.
- Amyloid ¥â-induced elevation of O-Glc N Acylated c-Fos promotes neuronal cell death. Aging Cell. (2019) 18(1):e12872.

   

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