Choonghee Lee

ORCID: 0000-0001-8907-5858
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Alzheimer's disease research and treatments
  • Gut microbiota and health
  • Tryptophan and brain disorders
  • Sleep and Wakefulness Research
  • Neurological Disease Mechanisms and Treatments
  • Inflammation biomarkers and pathways
  • Cholesterol and Lipid Metabolism
  • Sleep and related disorders
  • Immune cells in cancer
  • Cerebrovascular and genetic disorders
  • Cerebrospinal fluid and hydrocephalus
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Hormonal Regulation and Hypertension

Hope Center for Neurological Disorders
2022-2024

Washington University in St. Louis
2023-2024

University of Missouri–St. Louis
2023

Sleep loss is associated with cognitive decline in the aging population and a risk factor for Alzheimer’s disease (AD). Considering crucial role of immunomodulating genes such as that encoding triggering receptor expressed on myeloid cells type 2 (TREM2) removing pathogenic amyloid-β (Aβ) plaques regulating neurodegeneration brain, our aim was to investigate whether how sleep influences microglial function mice. We chronically sleep-deprived wild-type mice 5xFAD mouse model cerebral...

10.1126/scitranslmed.ade6285 article EN Science Translational Medicine 2023-04-26

Abstract It has recently become well-established that there is a connection between Alzheimer’s disease pathology and gut microbiome dysbiosis. We have previously demonstrated antibiotic-mediated microbiota perturbations lead to attenuation of Aβ deposition, phosphorylated tau accumulation, disease-associated glial cell phenotypes in sex-dependent manner. In this regard, we were intrigued by the finding marine-derived oligosaccharide, GV-971, was reported alter reduce amyloidosis 5XFAD mouse...

10.1186/s13024-023-00700-w article EN cc-by Molecular Neurodegeneration 2024-02-17

Alzheimer's disease (AD) is the most common cause of dementia. The APOE-ε4 allele apolipoprotein E (APOE) gene strongest genetic risk factor for late-onset AD. APOE genotype modulates effect sleep disruption on AD risk, suggesting a possible link between apoE and in pathogenesis, which relatively unexplored. We hypothesized that modifies Aβ deposition plaque-associated tau seeding spreading form neuritic plaque-tau (NP-tau) pathology response to chronic deprivation (SD) an isoform-dependent...

10.1172/jci169131 article EN cc-by Journal of Clinical Investigation 2023-06-06

Abstract Background Alzheimer Disease (AD) and cerebral amyloid angiopathy (CAA) are both characterized by amyloid-β (Aβ) accumulation in the brain, although Aβ deposits mostly brain parenchyma AD cerebrovasculature CAA. The presence of CAA can exacerbate clinical outcomes patients promoting spontaneous intracerebral hemorrhage ischemia leading to CAA-associated cognitive decline. Genetically, share ε4 allele apolipoprotein E ( APOE ) gene as strongest genetic risk factor. Although...

10.1186/s13024-023-00610-x article EN cc-by Molecular Neurodegeneration 2023-03-16

Parenchymal border macrophages (PBMs) reside close to the central nervous system parenchyma and regulate CSF flow dynamics. We recently demonstrated that PBMs provide a clearance pathway for amyloid-β peptide, which accumulates in brain Alzheimer’s disease (AD). Given emerging role AD, we explored how tau pathology affects PBM populations PS19 mouse model of pathology. reduction flow, an increase MHCII + subpopulation mice compared with WT littermates. Consequently, asked whether dysfunction...

10.26508/lsa.202302087 article EN cc-by Life Science Alliance 2023-08-10

Abstract Background Sleep disturbances are associated with the pathogenesis of neurodegenerative diseases including Alzheimer’s disease (AD) and primary tauopathies. We have previously shown that APOE4, strongest genetic risk factor for AD, directly influences severity key pathological hallmarks neurodegeneration tau deposition, microglial reactivity brain atrophy. loss accumulation in both mice humans, suggesting sleep may contribute to not only by influencing protein aggregation, but also...

10.1002/alz.089253 article EN cc-by Alzheimer s & Dementia 2024-12-01

Abstract It has recently become well-established that there is a connection between Alzheimer’s disease pathology and gut microbiome dysbiosis. We have previously demonstrated antibiotic-mediated microbiota perturbations lead to attenuation of Aβ deposition, phosphorylated tau accumulation, disease-associated glial cell phenotypes in sex-dependent manner. In this regard, we were intrigued by the finding marine-derived oligosaccharide, GV-971, was reported alter reduce amyloidosis mouse...

10.21203/rs.3.rs-3394003/v1 preprint EN cc-by Research Square (Research Square) 2023-10-09
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