ArticlePloS one2019
Glycosaminoglycans from Alzheimer's disease hippocampus have altered capacities to bind and regulate growth factors activities and to bind tau.
Article in PloS one, 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, 64 citations in OpenAlex.
- Decellularized matrix grafts and peripheral nerve regeneration.Neural regeneration research · 2026Article
- Application of Post-Glycosylation Modifying Enzymes for Mass Spectrometry Imaging of ModifiedJournal of the American Society for Mass Spectrometry · 2026Article
- Quantitative LC-MS/MS profiling reveals aberrant chondroitin sulfate in Alzheimer's disease.Communications biology · 2026Article
- Solvent Models and Charge Scaling: Benchmarks for Molecular Dynamics of Glycosaminoglycans.The journal of physical chemistry. B · 2026Article
- Signaling Pathways Triggering Therapeutical Potential of Marine-Derived Polysaccharides in Alzheimer's Disease: A Recent Review.Molecular neurobiology · 2026Review
- Characterization of Perineuronal Nets in the Human Cerebellum.Cerebellum (London, England) · 2025Article
- Multi-omic analysis of meningeal cerebral amyloid angiopathy reveals enrichment of unsubstituted glucosamine and extracellular proteins.Journal of neuropathology and experimental neurology · 2025Article
- A novel TGFβ1-Hs3st2-tau axis regulates tau pathology and synaptic integrity.Frontiers in neuroscience · 2025Article
- Novel Insights into Changes in Gene Expression within the Hypothalamus in Two Asthma Mouse Models: A Transcriptomic Lung-Brain Axis Study.International journal of molecular sciences · 2024Article
- FGFR3 drives Aβ-induced tau uptake.Experimental & molecular medicine · 2024Article
- Vascular Heparan Sulfate and Amyloid-β in Alzheimer's Disease Patients.International journal of molecular sciences · 2024Article
- Capturing biomarkers associated with Alzheimer disease subtypes using data distribution characteristics.Frontiers in computational neuroscience · 2024Article
- Global impact of proteoglycan science on human diseases.iScience · 2023Review
- Increased 3-Science advances · 2023Article
- A cationic motif upstream Engrailed2 homeodomain controls cell internalization through selective interaction with heparan sulfates.Nature communications · 2023Article
- Solvent Model Benchmark for Molecular Dynamics of Glycosaminoglycans.Journal of chemical information and modeling · 2023Article
- Heparan sulfate proteoglycan in Alzheimer's disease: aberrant expression and functions in molecular pathways related to amyloid-β metabolism.American journal of physiology. Cell physiology · 2023Review
- Heparan Sulfate Proteoglycans in Tauopathy.Biomolecules · 2022Review
- The Role of Extracellular Matrix in Human Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Heparan Sulfate and Sialic Acid in Viral Attachment: Two Sides of the Same Coin?International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycosaminoglycans (GAGs), including heparan sulfates and chondroitin sulfates, are major components of the extracellular matrix. Upon interacting with heparin binding growth factors (HBGF), GAGs participate to the maintaintenance of tissue homeostasis and contribute to self-healing. Although several processes regulated by HBGF are altered in Alzheimer's disease, it is unknown whether the brain GAG capacities to bind and regulate the function of HBGF or of other heparin binding proteins, as tau, are modified in this disease. Here, we show that total sulfated GAGs from hippocampus of Alzheimer's disease have altered capacities to bind and potentiate the activities of growth factors including FGF-2, VEGF, and BDNF while their capacity to bind to tau is remarkable increased. Alterations of GAG structures and capacities to interact with and regulate the activity of heparin binding proteins might contribute to impaired tissue homeostasis in the Alzheimer's disease brain.
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