ArticleActa neuropathologica2014
The role of pro-inflammatory S100A9 in Alzheimer's disease amyloid-neuroinflammatory cascade.
Article in Acta neuropathologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 86 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- Epigenetic scores of blood-based proteins as biomarkers of general cognitive function and brain health.Clinical epigenetics · 2024Pooled it
- The interplay between gut microbiota and Alzheimer's disease: mechanistic insights from dysbiosis to disease modulation.Metabolic brain disease · 2026Review
- Cyclosporine A Modulates Neuroinflammation-Related Gene Expression Associated with Alzheimer's Disease in SH-SY5Y Neuronal Cell Line: Is Cyclosporine A Beneficial/Detrimental?Biochemical genetics · 2026Article
- Plasma S100 Calcium-Binding Protein A8/A9 and Cognitive Impairment After Acute Ischemic Stroke.Journal of the American Heart Association · 2026Article
- Recent Advances in Polyoxometalates Targeting Proteins Associated with Alzheimer's Disease: From Molecular Mechanisms to Therapeutic Applications.International journal of molecular sciences · 2026Review
- CSF proteomic profiling with amyloid and tau pathology identifies distinctive sex-specific alteration of multiple proteins involved in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Can bacteria control the human brain?Communicative & integrative biology · 2026Review
- 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
- Mechanism of action and therapeutic potential of S100A8/A9 in neuroinflammation and cognitive impairment: From molecular target to clinical application (Review).International journal of molecular medicine · 2025Review
- Tau Enhances Aggregation of S100A9 Protein and Further Association of Its Fibrils.International journal of molecular sciences · 2025Article
- Navigation Between Alzheimer's Disease (AD) and Its Various Pathophysiological Trajectories: The Pathogenic Link to Neuroimmunology-Genetics and Neuroinflammation.International journal of molecular sciences · 2025Review
- Relationship of S100 Proteins with Neuroinflammation.Biomolecules · 2025Review
- Brain proteome changes after intracerebral hemorrhage in aged male and female mice.Neurobiology of disease · 2025Article
- Transcriptomic profile of microglia following inflammation-sensitized hypoxic-ischemic brain injury in neonatal rats suggests strong contribution to neutrophil chemotaxis and activation.Journal of neuroinflammation · 2025Article
- Edaravone-Dexborneol slows down pathological progression and cognitive decline via inhibiting S100A9 in APPswe/PS1dE9 mice.Alzheimer's research & therapy · 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
- Acute experimental colitis in 5xFAD Alzheimer's disease mice leads to enhanced monocyte infiltration into the brain accompanied by reduced β-amyloid deposition.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Importance of Gut Microbiota Dysbiosis and Circadian Disruption-Associated Biomarkers in Emergence of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Binding of Pro-Inflammatory Proteins S100A8 or S100A9 to Amyloid-β Peptide Suppresses Its Fibrillation.Biomolecules · 2025Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pro-inflammatory S100A9 protein is increasingly recognized as an important contributor to inflammation-related neurodegeneration. Here, we provide insights into S100A9 specific mechanisms of action in Alzheimer's disease (AD). Due to its inherent amyloidogenicity S100A9 contributes to amyloid plaque formation together with Aβ. In traumatic brain injury (TBI) S100A9 itself rapidly forms amyloid plaques, which were reactive with oligomer-specific antibodies, but not with Aβ and amyloid fibrillar antibodies. They may serve as precursor-plaques for AD, implicating TBI as an AD risk factor. S100A9 was observed in some hippocampal and cortical neurons in TBI, AD and non-demented aging. In vitro S100A9 forms neurotoxic linear and annular amyloids resembling Aβ protofilaments. S100A9 amyloid cytotoxicity and native S100A9 pro-inflammatory signaling can be mitigated by its co-aggregation with Aβ, which results in a variety of micron-scale amyloid complexes. NMR and molecular docking demonstrated transient interactions between native S100A9 and Aβ. Thus, abundantly present in AD brain pro-inflammatory S100A9, possessing also intrinsic amyloidogenic properties and ability to modulate Aβ aggregation, can serve as a link between the AD amyloid and neuroinflammatory cascades and as a prospective therapeutic target.
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Registered trials
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.