ArticleBrain pathology (Zurich, Switzerland)2008
Heparan sulfate accumulation with Abeta deposits in Alzheimer's disease and Tg2576 mice is contributed by glial cells.
Article in Brain pathology (Zurich, Switzerland), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 79 citations in OpenAlex.
- Co-Aggregation of Syndecan-3 with β-Amyloid Aggravates Neuroinflammation and Cognitive Impairment in 5×FAD Mice.International journal of molecular sciences · 2025Article
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- 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
- Design and Synthesis of 6-O-Phosphorylated Heparan Sulfate Oligosaccharides to Inhibit Amyloid β Aggregation.Chembiochem : a European journal of chemical biology · 2022Article
- Astrocytes and oligodendrocytes undergo subtype-specific transcriptional changes in Alzheimer's disease.Neuron · 2022Article
- Circadian control of heparan sulfate levels times phagocytosis of amyloid beta aggregates.PLoS genetics · 2022Article
- Isolation and Characterization of Heparan Sulfate Containing Amyloid Precursor Protein Degradation Products.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Integrated Genomic, Transcriptomic and Proteomic Analysis for Identifying Markers of Alzheimer's Disease.Diagnostics (Basel, Switzerland) · 2021Article
- Heparanase overexpression impedes perivascular clearance of amyloid-β from murine brain: relevance to Alzheimer's disease.Acta neuropathologica communications · 2021Article
- Glycosaminoglycans in Neurodegenerative Diseases.Advances in experimental medicine and biology · 2021Review
- Panoramic Visualization of Circulating MicroRNAs Across Neurodegenerative Diseases in Humans.Molecular neurobiology · 2019Article
- Article
- Systemic LPS-induced Aβ-solubilization and clearance in AβPP-transgenic mice is diminished by heparanase overexpression.Scientific reports · 2019Article
- The Expression, Regulation, and Biomarker Potential of Glypican-1 in Cancer.Frontiers in oncology · 2019Review
- Heparan sulfate S-domains and extracellular sulfatases (Sulfs): their possible roles in protein aggregation diseases.Glycoconjugate journal · 2018Review
- Heparan Sulfate Proteoglycans as Relays of Neuroinflammation.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Review
- Sulfated glycosaminoglycans in protein aggregation diseases.Glycoconjugate journal · 2017Review
- Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer's disease model.Molecular neurodegeneration · 2017Article
- The Alzheimer's disease risk factors apolipoprotein E and TREM2 are linked in a receptor signaling pathway.Journal of neuroinflammation · 2017Article
- Role of Matricellular Proteins in Disorders of the Central Nervous System.Neurochemical research · 2017Review
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14 authors at 1 institution in 1 country.
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Abstract
Amyloid beta-peptide (Abeta) plaques, one of the major neuropathological lesions in Alzheimer's disease (AD), can be broadly subdivided into two morphological categories: neuritic and diffuse. Heparan sulfate (HS) and HS proteoglycans (HSPGs) are codeposits of multiple amyloidoses, including AD. Although HS has been considered a limiting factor in the initiation of amyloid deposition, the pathological implications of HS in Abeta deposits of AD remain unclear. In this study, immunohistochemistry combined with fluorescence and confocal microscopy was employed to gain deeper insight into the accumulation of HS with Abeta plaques in sporadic and familial AD. Here we demonstrate that HS preferentially accumulated around the Abeta40 dense cores of neuritic plaques, but was largely absent from diffuse Abeta42 plaques, suggesting that Abeta42 deposition may occur independently of HS. A codeposition pattern of HS with Abeta deposits in Tg2576 mice was also examined. We identified the membrane-bound HSPGs, glypican-1 (GPC1) and syndecan-3 (SDC3), in glial cells associated with Abeta deposits, proximal to sites of HS accumulation. In mouse primary glial cultures, we observed increased levels of GPC1 and SDC3 following Abeta stimulation. These results suggest that HS codeposits with Abeta40 in neuritic plaques and is mainly derived from glial cells.
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