ArticlePloS one2011
Effects of heparin and enoxaparin on APP processing and Aβ production in primary cortical neurons from Tg2576 mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 31 citations in OpenAlex.
- Pathophysiological Role of Microglial Activation Induced by Blood-Borne Proteins in Alzheimer's Disease.Biomedicines · 2023Review
- Polysaccharides: potential bioactive macromolecules for Alzheimer's disease.Frontiers in nutrition · 2023Review
- In Silico Analysis of the Antagonist Effect of Enoxaparin on the ApoE4-Amyloid-Beta (ABiomolecules · 2022Article
- Repurposing food molecules as a potential BACE1 inhibitor for Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- A comprehensive guide to the pharmacologic regulation of angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 entry receptor.Pharmacology & therapeutics · 2021Review
- Glycosaminoglycan-Protein Interactions and Their Roles in Human Disease.Frontiers in molecular biosciences · 2021Review
- Overexpression of heparanase lowers the amyloid burden in amyloid-β precursor protein transgenic mice.The Journal of biological chemistry · 2015Article
- Role of cystatin C in amyloid precursor protein-induced proliferation of neural stem/progenitor cells.The Journal of biological chemistry · 2013Article
- Mannose-binding lectin binds to amyloid β protein and modulates inflammation.Journal of biomedicine & biotechnology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) is caused by accumulation of Aβ, which is produced through sequential cleavage of β-amyloid precursor protein (APP) by the β-site APP cleaving enzyme (BACE1) and γ-secretase. Enoxaparin, a low molecular weight form of the glycosaminoglycan (GAG) heparin, has been reported to lower Aβ plaque deposition and improve cognitive function in AD transgenic mice. METHODOLOGY/PRINCIPAL
findingsWe examined whether heparin and enoxaparin influence APP processing and inhibit Aβ production in primary cortical cell cultures. Heparin and enoxaparin were incubated with primary cortical cells derived from Tg2576 mice, and the level of APP and proteolytic products of APP (sAPPα, C99, C83 and Aβ) was measured by western blotting. Treatment of the cells with heparin or enoxaparin had no significant effect on the level of total APP. However, both GAGs decreased the level of C99 and C83, and inhibited sAPPα and Aβ secretion. Heparin also decreased the level of β-secretase (BACE1) and α-secretase (ADAM10). In contrast, heparin had no effect on the level of ADAM17. CONCLUSIONS/SIGNIFICANCE: The data indicate that heparin and enoxaparin decrease APP processing via both α- and β-secretase pathways. The possibility that GAGs may be beneficial for the treatment of AD needs further study.
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