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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, HJ[Kim, Hee Jin]; Chang, KA[Chang, Keun-A]; Ha, TY[Ha, Tae-Young]; Kim, J[Kim, Jeonga]; Ha, S[Ha, Sungji]; Shin, KY[Shin, Ki-Young]; Moon, C[Moon, Cheil]; Nacken, W[Nacken, Wolfgang]; Kim, HS[Kim, Hye-Sun]; Suh, YH[Suh, Yoo-Hun]
- DGIST Authors
- Moon, C[Moon, Cheil]
- Issue Date
- PLoS ONE, 9(2)
- Article Type
- Alzheimer' s Disease (AD); Amyloid Beta-Peptides; Amyloid Beta Protein; Amyloid Precursor Protein; Animal; Animal Cell; Animal Experiment; Animal Model; Animal Tissue; Animals; C57Bl Mouse; Calgranulin B; Carboxy Terminal Sequence; Cognition Disorders; Cognitive Defect; Controlled Study; Cross Breeding; Degenerative Disease; Disease Model; Disease Models, Animal; Female; Gene Inactivation; Genetics; Interleukin-10; Interleukin-6; Knockout Mouse; Male; Memory Disorder; Memory Disorders; Mental Task; Metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Morris Water Maze Test; Mouse; Neurodegenerative Diseases; Neuropathology; Non-Human; Pathophysiology; Protein Expression; Protein Phosphorylation; Reference Memory; S100A9 Gene; S100A9 Protein, Mouse; Spatial Memory; Tau Protein; Tg2576 Mouse; Transgenic Mouse; Tumor 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
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- Brain and Cognitive SciencesMoon Lab1. Journal Articles
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