S100A9 Knockout Decreases the Memory Impairment and Neuropathology in Crossbreed Mice of Tg2576 and S100A9 Knockout Mice ModelS100A9 Knockout Decreases the Memory Impairment and Neuropathology in Crossbreed Mice of Tg2576 and S100A9 Knockout Mice Model
- Other Titles
- S100A9 Knockout Decreases the Memory Impairment and Neuropathology in Crossbreed Mice of Tg2576 and S100A9 Knockout Mice Model
- Authors
- 김희진; 장근아; 하태영; 김정아; 하성지; 신기영; 문제일; Wolfgang Nacken; 김혜선; 서유헌
- Issue Date
- Feb-2014
- Publisher
- Public Library of Science
- Citation
- PLoS ONE, v.9, no.2, pp.e88924
- Journal Title
- PLoS ONE
- Volume
- 9
- Number
- 2
- Start Page
- e88924
- URI
- http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/958
- DOI
- 10.1371/journal.pone.0088924
- ISSN
- 1932-6203
- Abstract
- 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 (Ab) neuropathology because of reduced levels of A beta, 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)-alpha 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.
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