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S100A9 Knockout Decreases the Memory Impairment and Neuropathology in Crossbreed Mice of Tg2576 and S100A9 Knockout Mice Model

S100A9 Knockout Decreases the Memory Impairment and Neuropathology in Crossbreed Mice of Tg2576 and S100A9 Knockout Mice Model
Kim, Hee JinChang, Keun-AHa, Tae-YoungKim, JeongaHa, SungjiShin, Ki-YoungMoon, CheilNacken, WolfgangKim, Hye-SunSuh, Yoo-Hun
DGIST Authors
Moon, Cheil
Issue Date
PLoS ONE, 9(2)
Article Type
Alzheimer&aposs Disease (AD)Amyloid Beta-PeptidesAmyloid Beta ProteinAmyloid Precursor ProteinAnimalAnimal CellAnimal ExperimentAnimal ModelAnimal TissueAnimalsC57Bl MouseCalgranulin BCarboxy Terminal SequenceCognition DisordersCognitive DefectControlled StudyCross BreedingDegenerative DiseaseDisease ModelDisease Models, AnimalFemaleGene InactivationGeneticsInterleukin-10Interleukin-6Knockout MouseMaleMemory DisorderMemory DisordersMental TaskMetabolismMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMorris Water Maze TestMouseNeurodegenerative DiseasesNeuropathologyNon-HumanPathophysiologyProtein ExpressionProtein PhosphorylationReference MemoryS100A9 GeneS100A9 Protein, MouseSpatial MemoryTau ProteinTg2576 MouseTransgenic MouseTumor Necrosis Factor-Alpha
Our previous study presented evidence that the inflammation-related S100A9 gene is significantly upregulated in the brains of Alzheimer's disease (AD) animal models and human AD patients. In addition, experiments have shown that knockdown of S100A9 expression improves cognition function in AD model mice (Tg2576), and these animals exhibit reduced amyloid plaque burden. In this study, we established a new transgenic animal model of AD by crossbreeding the Tg2576 mouse with the S100A9 knockout (KO) mouse. We observed that S100A9KO/Tg2576 (KO/Tg) mice displayed an increased spatial reference memory in the Morris water maze task and Y-maze task as well as decreased amyloid beta peptide (Aβ) neuropathology because of reduced levels of Aβ, C-terminal fragments of amyloid precursor protein (APP-CT) and phosphorylated tau and increased expression of anti-inflammatory IL-10 and also decreased expression of inflammatory IL-6 and tumor neurosis factor (TNF)-α when compared with age-matched S100A9WT/Tg2576 (WT/Tg) mice. Overall, these results suggest that S100A9 is responsible for the neurodegeneration and cognitive deficits in Tg2576 mice. The mechanism of S100A9 is able to coincide with the inflammatory process. These findings indicate that knockout of S100A9 is a potential target for the pharmacological therapy of AD. © 2014 Kim et al.
Public Library of Science
Related Researcher
  • Author Moon, Cheil Moon Lab
  • Research Interests Brain convergent science based on chemical senses; olfaction; 감각신경계 기반 뇌융합과학; 후각 신경계
Department of Brain and Cognitive SciencesMoon Lab1. Journal Articles

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