ArticleJournal of neuropathology and experimental neurology2011
Changes in brain β-amyloid deposition and aquaporin 4 levels in response to altered agrin expression in mice.
Article in Journal of neuropathology and experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 56 citations in OpenAlex.
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- Biomimetic strategies for the deputization of proteoglycan functions.Frontiers in cell and developmental biology · 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
- Urinary protein biomarkers based on LC-MS/MS analysis to discriminate vascular dementia from Alzheimer's disease in Han Chinese population.Frontiers in aging neuroscience · 2023Article
- Analysis of Cerebral Small Vessel Changes in AD Model Mice.Biomedicines · 2022Article
- The amyloid plaque proteome in early onset Alzheimer's disease and Down syndrome.Acta neuropathologica communications · 2022Article
- Emerging roles for dynamic aquaporin-4 subcellular relocalization in CNS water homeostasis.Brain : a journal of neurology · 2022Article
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- The mechanisms underlying the actions of Xuefu Zhuyu decoction pretreatment against neurological deficits after ischemic stroke in mice: The mediation of glymphatic function by aquaporin-4 and its anchoring proteins.Frontiers in pharmacology · 2022Article
- Blood-Brain Barrier Alterations and Edema Formation in Different Brain Mass Lesions.Frontiers in cellular neuroscience · 2022Review
- The Role of Extracellular Matrix Components in the Spreading of Pathological Protein Aggregates.Frontiers in cellular neuroscience · 2022Review
- Basal lamina changes in neurodegenerative disorders.Molecular neurodegeneration · 2021Review
- Extracellular protein components of amyloid plaques and their roles in Alzheimer's disease pathology.Molecular neurodegeneration · 2021Review
- Integration of System Biology Tools to Investigate Huperzine A as an Anti-Alzheimer Agent.Frontiers in pharmacology · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
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Abstract
Conditions that compromise the blood-brain barrier (BBB) have been increasingly implicated in the pathogenesis of Alzheimer disease (AD). AGRIN is a heparan sulfate proteoglycan found abundantly in basement membranes of the cerebral vasculature, where it has been proposed to serve a functional role in the BBB. Furthermore, AGRIN is the major heparan sulfate proteoglycan associated with amyloid plaques in AD brains. To examine the relationship of AGRIN, the BBB, and AD-related pathologies, we generated mice in which the Agrn gene was deleted from either endothelial cells or neurons using gene targeting or was overexpressed using a genomic transgene construct. These mice were combined with a transgenic model of AD that over expresses disease-associated forms of amyloid precursor protein and presenilin 1. In mice lacking endothelial cell expression of Agrn, the BBB remained intact but aquaporin 4 levels were reduced, indicating that the loss of AGRIN affects BBB-associated components. This change in Agrn resulted in an increase in β-amyloid (Aβ) in the brain. Conversely, overexpression of Agrn decreased Aβ deposition, whereas elimination of Agrn from neurons did not change Aβ levels. These results indicate that AGRIN is important for maintaining BBB composition and that changes in Agrn expression (particularly vessel-associated AGRIN) influence Aβ homeostasis in mouse models of AD.
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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.