ArticleScientific reports2018
S100A9-Driven Amyloid-Neuroinflammatory Cascade in Traumatic Brain Injury as a Precursor State for Alzheimer's Disease.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
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- ARMH4 accelerates aging by maintaining a positive-feedback growth signaling circuit.Nature communications · 2025Article
- The molecular architecture of severe pediatric traumatic brain injury: integrated omics reveal therapeutic pathways.Critical care (London, England) · 2025Observational
- Targeted S100A8 PP-Cas9@PLGA-apt microparticles reduced cartilage degradation and subchondral bone isomerism in osteoarthritis treatment through JAK/STAT3 pathway modulation.Materials today. Bio · 2025Article
- Proteome-Based Biomarkers for Alzheimer's Disease: Old Acquisitions and Innovative Proposals.International journal of molecular sciences · 2025Review
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- Calcium-Dependent S100A8 Amyloid Fibril Formation via S100A1-Mediated Transient Interaction.ACS chemical neuroscience · 2025Article
- Heterotypic Droplet Formation by Pro-Inflammatory S100A9 and Neurodegenerative Disease-Related α-Synuclein.Biomacromolecules · 2025Article
- Effect of Glutamate Antibodies on ASCL1 Gene Expression in Aging Mice with Spatial Memory Impairment Caused by Amyloid Fibrils of the Proinflammatory Protein S100A9.Bulletin of experimental biology and medicine · 2025Article
- Binding of Pro-Inflammatory Proteins S100A8 or S100A9 to Amyloid-β Peptide Suppresses Its Fibrillation.Biomolecules · 2025Article
- Pro-inflammatory S100A9 contributes to retinal ganglion cell degeneration in glaucoma.Frontiers in immunology · 2025Article
- Changing expression system alters oligomerization and proinflammatory activity of recombinant human S100A9.bioRxiv : the preprint server for biology · 2024Article
- Association study of S100A9 gene polymorphisms with Parkinson's disease risk and age of disease onset.Acta neurologica Belgica · 2024Article
- Formation of Calprotectin Inhibits Amyloid Aggregation of S100A8 and S100A9 Proteins.ACS chemical neuroscience · 2024Article
- Locus coeruleus injury modulates ventral midbrain neuroinflammation during DSS-induced colitis.Research square · 2024Article
- ApoE Isoforms Inhibit Amyloid Aggregation of Proinflammatory Protein S100A9.International journal of molecular sciences · 2024Article
- Endogenous Ligands of TLR4 in Microglia: Potential Targets for Related Neurological Diseases.Current drug targets · 2024Review
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Corrections and comments
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Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pro-inflammatory and amyloidogenic S100A9 protein is an important contributor to Alzheimer's disease (AD) pathology. Traumatic brain injury (TBI) is viewed as a precursor state for AD. Here we have shown that S100A9-driven amyloid-neuroinflammatory cascade was initiated in TBI and may serve as a mechanistic link between TBI and AD. By analyzing the TBI and AD human brain tissues, we demonstrated that in post-TBI tissues S100A9, produced by neurons and microglia, becomes drastically abundant compared to Aβ and contributes to both precursor-plaque formation and intracellular amyloid oligomerization. Conditions implicated in TBI, such as elevated S100A9 concentration, acidification and fever, provide strong positive feedback for S100A9 nucleation-dependent amyloid formation and delay in its proteinase clearance. Consequently, both intracellular and extracellular S100A9 oligomerization correlated with TBI secondary neuronal loss. Common morphology of TBI and AD plaques indicated their similar initiation around multiple aggregation centers. Importantly, in AD and TBI we found S100A9 plaques without Aβ. S100A9 and Aβ plaque pathology was significantly advanced in AD cases with TBI history at earlier age, signifying TBI as a risk factor. These new findings highlight the detrimental consequences of prolonged post-TBI neuroinflammation, which can sustain S100A9-driven amyloid-neurodegenerative cascade as a specific mechanism leading to AD development.
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