ArticlePloS one2014
S100A9 knockout decreases the memory impairment and neuropathology in crossbreed mice of Tg2576 and S100A9 knockout mice model.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Plasma S100 Calcium-Binding Protein A8/A9 and Cognitive Impairment After Acute Ischemic Stroke.Journal of the American Heart Association · 2026Article
- Dysbiosis and the gut-brain axis impairment in the pathophysiology of Alzheimer's disease and related dementias: is 'pathobiome' an etiological element?Essays in biochemistry · 2025Review
- Edaravone-Dexborneol slows down pathological progression and cognitive decline via inhibiting S100A9 in APPswe/PS1dE9 mice.Alzheimer's research & therapy · 2025Article
- Pro-inflammatory S100A9 contributes to retinal ganglion cell degeneration in glaucoma.Frontiers in immunology · 2025Article
- Association study of S100A9 gene polymorphisms with Parkinson's disease risk and age of disease onset.Acta neurologica Belgica · 2024Article
- The Stabilization of S100A9 Structure by Calcium Inhibits the Formation of Amyloid Fibrils.International journal of molecular sciences · 2023Article
- The Role of Macrophage Populations in Skeletal Muscle Insulin Sensitivity: Current Understanding and Implications.International journal of molecular sciences · 2023Review
- Review
- TLR9 Mediates Periodontal Aging by Fostering Senescence and Inflammaging.Journal of dental research · 2022Article
- Selecting Multitarget Peptides for Alzheimer's Disease.Biomolecules · 2022Article
- Rapamycin-filgrastim combination therapy ameliorates portal hypertension-induced splenomegaly: Role of β actin and S100A9 proteins modulation.Iranian journal of basic medical sciences · 2022Article
- Genetic Inactivation of Free Fatty Acid Receptor 3 Impedes Behavioral Deficits and Pathological Hallmarks in the APPInternational journal of molecular sciences · 2022Article
- Human microRNA-4433 (hsa-miR-4443) Targets 18 Genes to be a Risk Factor of Neurodegenerative Diseases.Current Alzheimer research · 2022Article
- S100a9 Protects Male Lupus-Prone NZBWF1 Mice From Disease Development.Frontiers in immunology · 2021Article
- Modulation of KDM1A with vafidemstat rescues memory deficit and behavioral alterations.PloS one · 2020Article
- S100A8/A9 Drives Neuroinflammatory Priming and Protects against Anxiety-like Behavior after Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Effects of a Dehydroevodiamine-Derivative on Synaptic Destabilization and Memory Impairment in the 5xFAD, Alzheimer's Disease Mouse Model.Frontiers in behavioral neuroscience · 2018Article
- Histone Deacetylase Inhibitor Alleviates the Neurodegenerative Phenotypes and Histone Dysregulation in Presenilins-Deficient Mice.Frontiers in aging neuroscience · 2018Article
- S100A6 protein: functional roles.Cellular and molecular life sciences : CMLS · 2017Review
- Blast exposure causes dynamic microglial/macrophage responses and microdomains of brain microvessel dysfunction.Neuroscience · 2016Article
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10 authors.
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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 (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.
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