ArticleJournal of Alzheimer's disease : JAD2019
Increased Hyaluronan and TSG-6 in Association with Neuropathologic Changes of Alzheimer's Disease.
Article in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- Extracellular matrix remodeling therapeutic strategies to tackle central nervous system diseases.Neural regeneration research · 2026Article
- Quantitative LC-MS/MS profiling reveals aberrant chondroitin sulfate in Alzheimer's disease.Communications biology · 2026Article
- Lecanemab alters basement membrane collagen IV in viable microvessels isolated from brains with high Alzheimer's disease neuropathology.Journal of Alzheimer's disease : JAD · 2026Article
- Epigenetic Regulation of Hyaluronan-Associated Genes in the Brain: Identifying Key Regulatory Sites.Epigenomes · 2026Review
- Taking its TOLL: the role of toll-like receptor 4 in human health and disease, and its potential as a therapeutic target.Frontiers in immunology · 2026Review
- Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy.Frontiers in pharmacology · 2026Review
- Brain Endothelial Glycocalyx as a Blood-Facing Translational Interface in Alzheimer's Disease: Beyond "Leaky" Barriers Toward Repair-First Stratification.Drug design, development and therapy · 2026Review
- HAPLN2 forms aggregates and promotes microglial inflammation during brain aging in mice.PLoS biology · 2025Article
- In Vivo Cortical Microstructure: Relationships With Tauopathy and Cognitive Impairment in the Elderly.Journal of neurochemistry · 2025Article
- Hyaluronidases as Targets for the Treatment of Neurological Diseases.Proteoglycan research · 2025Article
- TSG-6 Protects Against Cerebral Ischemia-Reperfusion Injury via Upregulating Hsp70-1B in Astrocytes.CNS neuroscience & therapeutics · 2025Article
- Potential drug targets for ovarian cancer identified through Mendelian randomization and colocalization analysis.Journal of ovarian research · 2025Article
- The role of extracellular matrix viscoelasticity in development and disease.npj biological physics and mechanics · 2025Review
- Brain Ischemic Tolerance Triggered by Preconditioning Involves Modulation of Tumor Necrosis Factor-α-Stimulated Gene 6 (TSG-6) in Mice Subjected to Transient Middle Cerebral Artery Occlusion.Current issues in molecular biology · 2024Article
- Microvascular and cellular dysfunctions in Alzheimer's disease: an integrative analysis perspective.Scientific reports · 2024Article
- Inter-alpha-trypsin inhibitor (IαI) and hyaluronan modifications enhance the innate immune response to influenza virus in the lung.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Unraveling neurovascular mysteries: the role of endothelial glycocalyx dysfunction in Alzheimer's disease pathogenesis.Frontiers in physiology · 2024Review
- Research Progress on Natural Plant Molecules in Regulating the Blood-Brain Barrier in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Review
- Endothelial Glycocalyx in Aging and Age-related Diseases.Aging and disease · 2023Review
- Characterization of the Involvement of Tumour Necrosis Factor (TNF)-α-Stimulated Gene 6 (TSG-6) in Ischemic Brain Injury Caused by Middle Cerebral Artery Occlusion in Mouse.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Little is known about the extracellular matrix (ECM) during progression of AD pathology. Brain ECM is abundant in hyaluronan (HA), a non-sulfated glycosaminoglycan synthesized by HA synthases (HAS) 1-3 in a high molecular weight (MW) form that is degraded into lower MW fragments. We hypothesized that pathologic severity of AD is associated with increases in HA and HA-associated ECM molecules. To test this hypothesis, we assessed HA accumulation and size; HA synthases (HAS) 1-3; and the HA-stabilizing hyaladherin, TSG-6 in parietal cortex samples from autopsied research subjects with not AD (CERAD = 0, Braak = 0- II, n = 12-21), intermediate AD (CERAD = 2, Braak = III-IV, n = 13-18), and high AD (CERAD = 3, Braak = V-VI, n = 32-40) neuropathologic change. By histochemistry, HA was associated with deposits of amyloid and tau, and was also found diffusely in brain parenchyma, with overall HA quantity (measured by ELSA) significantly greater in brains with high AD neuropathology. Mean HA MW was similar among the samples. HAS2 and TSG-6 mRNA expression, and TSG-6 protein levels were significantly increased in high AD and both molecules were present in vasculature, NeuN-positive neurons, and Iba1-positive microglia. These results did not change when accounting for gender, advanced age (≥ 90 years versus <90 years), or the clinical diagnosis of dementia. Collectively, our results indicate a positive correlation between HA accumulation and AD neuropathology, and suggest a possible role for HA synthesis and metabolism in AD progression.
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Registered trials
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