A5084764379- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Receptors and Signaling
- Autophagy in Disease and Therapy
- Mitochondrial Function and Pathology
- Immune cells in cancer
- Dyeing and Modifying Textile Fibers
- Viral Infectious Diseases and Gene Expression in Insects
- Collagen: Extraction and Characterization
- Virus-based gene therapy research
- Parkinson's Disease Mechanisms and Treatments
- Chemokine receptors and signaling
- Echinoderm biology and ecology
- Animal Virus Infections Studies
- Invertebrate Immune Response Mechanisms
- Advanced Glycation End Products research
- Genetic Neurodegenerative Diseases
- Endoplasmic Reticulum Stress and Disease
- Skin Protection and Aging
- Microbial Metabolic Engineering and Bioproduction
- Physiological and biochemical adaptations
Gladstone Institutes
2023-2024
University of California, San Francisco
2023-2024
Stanford University
2018-2021
Gyeongsang National University
2016
Apolipoprotein E4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD), leading to earlier age of clinical onset and exacerbating pathologies. There a critical need identify protective targets. Recently, rare APOE variant, APOE3-R136S (Christchurch), was found protect against early-onset AD in PSEN1-E280A carrier. In this study, we sought determine if R136S mutation also protects APOE4-driven effects LOAD. We generated tauopathy mouse human iPSC-derived...
Despite strong evidence supporting the important roles of both apolipoprotein E4 (APOE4) and microglia in Alzheimer's disease (AD) pathogenesis, effects on neuronal APOE4-related AD pathogenesis remain elusive. To examine such effects, we utilized microglial depletion a chimeric model with induced pluripotent stem cell (iPSC)-derived human neurons mouse hippocampus. Specifically, transplanted homozygous APOE4, isogenic APOE3, APOE-knockout (APOE-KO) iPSC-derived into hippocampus APOE3 or...
Apolipoprotein E4 (APOE4) is an important driver of Tau pathology, gliosis, and degeneration in Alzheimer's disease (AD). Still, the mechanisms underlying these APOE4-driven pathological effects remain elusive. Here, we report a tauopathy mouse model that APOE4 promoted nucleocytoplasmic translocation release high-mobility group box 1 (HMGB1) from hippocampal neurons, which correlated with severity microgliosis degeneration. Injection HMGB1 into hippocampus young APOE4-tauopathy mice induced...
Despite strong evidence supporting the involvement of both apolipoprotein E4 (APOE4) and microglia in Alzheimer's Disease (AD) pathogenesis, effects on neuronal APOE4-driven AD pathogenesis remain elusive. Here, we examined such utilizing microglial depletion a chimeric model with human neurons mouse hippocampus. Specifically, transplanted homozygous APOE4, isogenic APOE3, APOE-knockout (APOE-KO) induced pluripotent stem cell (iPSC)-derived into hippocampus APOE3 or APOE4 knock-in mice,...
The fly trachea is the equivalent of mammalian lung and a useful model for human respiratory diseases. However, little known about molecular mechanisms underlying tracheal air filling during larval development. In this study, we discover that PTPMT1 has function in filling. widely conserved, ubiquitously expressed mitochondrial phosphatase. To reveal PTPMT1's functions genetically tractable invertebrates whether those are tissue specific, generate Drosophila depletion. We find mutants show...