ArticleJournal of neuroinflammation2016
Suppression of LPS-induced tau hyperphosphorylation by serum amyloid A.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
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- Serum Amyloid A3 Expression Is Enhanced by Gram-Negative Bacterial Stimuli in Bovine Endometrial Epithelial Cells.Pathogens (Basel, Switzerland) · 2025Article
- Mapping the hippocampal spatial proteomic signature in male and female mice of an early Alzheimer's disease model.Biology of sex differences · 2025Article
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- Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.International journal of molecular sciences · 2025Review
- Gut microbiome-derived metabolites in Alzheimer's disease: Regulation of immunity and potential for therapeutics.Immunological reviews · 2024Review
- Interactions of Serum Amyloid A Proteins with the Blood-Brain Barrier: Implications for Central Nervous System Disease.International journal of molecular sciences · 2024Review
- The endotoxin hypothesis of Alzheimer's disease.Molecular neurodegeneration · 2024Review
- Early-Stage Moderate Alcohol Feeding Dysregulates Insulin-Related Metabolic Hormone Expression in the Brain: Potential Links to Neurodegeneration Including Alzheimer's Disease.Journal of Alzheimer's disease reports · 2024Article
- Catechin Protects against Lipopolysaccharide-induced Depressive-like Behaviour in Mice by Regulating Neuronal and Inflammatory Genes.Current gene therapy · 2024Article
- Extended range proteomic analysis of blood plasma from schizophrenia patients.Frontiers in molecular biosciences · 2024Article
- Severity of Peripheral Infection Differentially Affects Brain Functions in Mice via Microglia-Dependent and -Independent Mechanisms.International journal of molecular sciences · 2023Article
- Tau and neuroinflammation in Alzheimer's disease: interplay mechanisms and clinical translation.Journal of neuroinflammation · 2023Review
- Minocycline Attenuates Lipopolysaccharide-Induced Locomotor Deficit and Anxiety-like Behavior and Related Expression of the BDNF/CREB Protein in the Rat Medial Prefrontal Cortex (mPFC).International journal of molecular sciences · 2022Article
- Multi-Omics, an Integrated Approach to Identify Novel Blood Biomarkers of Alzheimer's Disease.Metabolites · 2022Article
- The Chemerin/CMKLR1 Axis Is Involved in the Recruitment of Microglia to Aβ Deposition through p38 MAPK Pathway.International journal of molecular sciences · 2022Article
- Adolescent Binge Alcohol Enhances Early Alzheimer's Disease Pathology in Adulthood Through Proinflammatory Neuroimmune Activation.Frontiers in pharmacology · 2022Article
- Acupuncture Effect Assessment in APP/PS1 Transgenic Mice: On Regulating Learning-Memory Abilities, Gut Microbiota, and Microbial Metabolites.Computational and mathematical methods in medicine · 2022Article
- Chronic Ethanol Causes Persistent Increases in Alzheimer's Tau Pathology in Female 3xTg-AD Mice: A Potential Role for Lysosomal Impairment.Frontiers in behavioral neuroscience · 2022Article
- Gram-negative bacteria and their lipopolysaccharides in Alzheimer's disease: pathologic roles and therapeutic implications.Translational neurodegeneration · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulation of hyperphosphorylated tau is a major neuropathological feature of tauopathies including Alzheimer's disease (AD). Serum amyloid A (SAA), an acute-phase protein with cytokine-like property, has been implicated in amyloid deposition. It remains unclear whether SAA affects tau hyperphosphorylation.
methodsPotential involvement of SAA in tau hyperphosphorylation was examined using intracerebral injection of SAA, and in Saa3 (-/-) mice receiving systemic administration of lipopolysaccharide (LPS). Induced SAA expression and microglial activation were evaluated in these mice using real-time PCR and/or immunofluorescence staining. Cultured primary neuronal cells were treated with condition media (CM) from SAA-stimulated primary microglial cells. The alteration in tau hyperphosphorylation was determined using Western blotting.
resultsSaa3 is the predominant form of SAA proteins induced by LPS in the mouse brain that co-localizes with neurons. Overexpression of SAA by intracerebral injection attenuated tau hyperphosphorylation in the brain. Conversely, Saa3 deficiency enhanced tau phosphorylation induced by systemic LPS administration. Intracerebral injection of SAA also induced the activation of microglia in the brains. IL-10 released to CM from SAA-stimulated microglia attenuated tau hyperphosphorylation in cultured primary neurons. IL-10 neutralizing antibody reversed the effect of SAA in the attenuation of tau phosphorylation.
conclusionsLPS-induced expression of SAA proteins in the brain leads to the activation of microglia and release of IL-10, which in turn suppresses tau hyperphosphorylation in a mouse model of systemic inflammation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.