ArticleJournal of neurochemistry2013
Increased prion protein processing and expression of metabotropic glutamate receptor 1 in a mouse model of Alzheimer's disease.
Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- A genome wide association study links glutamate receptor pathway to sporadic Creutzfeldt-Jakob disease risk.PloS one · 2014Pooled it
- Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Anchorless risk or released benefit? An updated view on the ADAM10-mediated shedding of the prion protein.Cell and tissue research · 2023Review
- mGluR1α expression in the hippocampus, subiculum, entorhinal cortex and superior temporal gyrus in Alzheimer's disease.IBRO neuroscience reports · 2022Article
- Article
- Early Effects of the Soluble Amyloid βInternational journal of molecular sciences · 2021Article
- Review
- Amyloid Fibril-Induced Astrocytic Glutamate Transporter Disruption Contributes to Complement C1q-Mediated Microglial Pruning of Glutamatergic Synapses.Molecular neurobiology · 2020Article
- Brain tumor acidification using drugs simultaneously targeting multiple pH regulatory mechanisms.Journal of neuro-oncology · 2019Article
- Activation of mGluR1 Mediates C1q-Dependent Microglial Phagocytosis of Glutamatergic Synapses in Alzheimer's Rodent Models.Molecular neurobiology · 2019Article
- Fragile X and APP: a Decade in Review, a Vision for the Future.Molecular neurobiology · 2019Review
- Unchanged type 1 metabotropic glutamate receptor availability in patients with Alzheimer's disease: A study usingNeuroImage. Clinical · 2019Article
- Detection of Active Caspase-3 in Mouse Models of Stroke and Alzheimer's Disease with a Novel Dual Positron Emission Tomography/Fluorescent Tracer [Contrast media & molecular imaging · 2019Article
- Prions, prionoids and protein misfolding disorders.Nature reviews. Genetics · 2018Review
- Prion Proteins Without the Glycophosphatidylinositol Anchor: Potential Biomarkers in Neurodegenerative Diseases.Biomarker insights · 2018Review
- Inhibition of group-I metabotropic glutamate receptors protects against prion toxicity.PLoS pathogens · 2017Article
- Regulation of Amyloid β Oligomer Binding to Neurons and Neurotoxicity by the Prion Protein-mGluR5 Complex.The Journal of biological chemistry · 2016Article
- The Transient Receptor Potential Melastatin 2 (TRPM2) Channel Contributes to β-Amyloid Oligomer-Related Neurotoxicity and Memory Impairment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Article
- Metabotropic glutamate receptor 5 knockout reduces cognitive impairment and pathogenesis in a mouse model of Alzheimer's disease.Molecular brain · 2014Article
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9 authors at 2 institutions in 2 countries.
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Abstract
Prion protein (PrP(C) ), a glycosylphosphatidylinositol-anchored protein corrupted in prion diseases, has been shown recently to interact with group I metabotropic glutamate receptors (mGluRs). Moreover, both PrP(C) and mGluRs were proposed to function as putative receptors for β-amyloid in Alzheimer's disease. PrP(C) can be processed in neurons via α or β-cleavage to produce PrP(C) fragments that are neuroprotective or toxic, respectively. We found PrP(C) α-cleavage to be 2-3 times higher in the cortex of APPswe/PS1dE9 mice, a mouse model of Alzheimer's disease. A similar age-dependent increase was observed for PrP(C) β-cleavage. Moreover, we observed considerable age-dependent increase in cortical expression of mGluR1, but not mGluR5. Exposure of cortical neuronal cultures to β-amyloid oligomers upregulated mGluR1 and PrP(C) α-cleavage, while activation of group I mGluRs increased PrP(C) shedding from the membrane, likely due to increased levels of a disintegrin and metalloprotease10, a key disintegrin for PrP(C) shedding. Interestingly, a similar increase in a disintegrin and metalloprotease10 was detected in the cortex of 9-month-old APPswe/PS1dE9 animals. Our experiments reveal novel and complex processing of PrP(C) in connection with mGluR overexpression that seems to be triggered by β-amyloid peptides. Prion protein (PrP(C) ) and metabotropic glutamate receptors (mGluR) are implicated in Alzheimer's disease (AD). We found age-dependent increase in PrP(C) processing, ADAM10 and mGluR1 levels in AD mouse model. These changes could be reproduced in cultured cortical neurons treated with Aβ peptide. Our findings suggest that increased levels of Aβ can trigger compensatory responses that may affect neuronal toxicity.
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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.