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Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein
Open accessAbstract
Soluble amyloid-β oligomers (Aβo) trigger Alzheimer's disease (AD) pathophysiology and bind with high affinity to cellular prion protein (PrP(C)). At the postsynaptic density (PSD), extracellular Aβo bound to lipid-anchored PrP(C) activates intracellular Fyn kinase to disrupt synapses. Here, we screened transmembrane PSD proteins heterologously for the ability to couple Aβo-PrP(C) with Fyn. Only coexpression of the metabotropic glutamate receptor, mGluR5, allowed PrP(C)-bound Aβo to activate Fyn. PrP(C) and mGluR5 interact physically, and cytoplasmic Fyn forms a complex with mGluR5. Aβo-PrP(C) generates mGluR5-mediated increases of intracellular calcium in Xenopus oocytes and in neurons, and the latter is also driven by human AD brain extracts. In addition, signaling by Aβo-PrP(C)-mGluR5 complexes mediates eEF2 phosphorylation and dendritic spine loss. For mice expressing familial AD transgenes, mGluR5 antagonism reverses deficits in learning, memory, and synapse density. Thus, Aβo-PrP(C) complexes at the neuronal surface activate mGluR5 to disrupt neuronal function.
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“Aβ oligomers can drive additional vicious cycles by stimulating metabotropic glutamate receptor 5 (mGluR5)146,147, which activates feedforward Ca2+–cAMP signaling and drive tau phosphorylation (Fig. 5, brown).”
From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [147]
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“Amyloid-β oligomer binding results in aberrant neuronal signaling and the endocytosis of the dysfunctional synapse into the cell [126,127].”
From Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases (2023) · cites this paper as [126]
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“Among the Aβ binding candidates, cellular prion protein (PrPc) represents the most studied, either alone or through a complex with mGluR5 [37, 62, 72, 79].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [72]
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“The most studied binding partner is the PrPc, which through a cascade involving a complex with mGluR5 may lead to toxicity independently or via tau [37, 62, 72, 79].”
From Transmembrane protein 97 is a potential synaptic amyloid beta receptor in human Alzheimer’s disease (2024) · cites this paper as [72]
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“Amyloid-β oligomers bind to a protein complex comprised of cellular prion protein (PrPc) along with other proteins including leukocyte immunoglobulin-like receptor subfamily B2/paired immunoglobulin-like type 2 receptor B (LilrB2), and possibly also Nogo-66 receptor 1 (Nogo-1), low-affinity nerve growth factor (NGF) receptor [125] (Figure 3), and the metabotropic glutamate receptor 5 [126].”
From Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases (2023) · cites this paper as [126]
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Metadata
- Authors
- Um, J. W., Kaufman, A. C., Kostylev, M., Heiss, J. K., Stagi, M., Takahashi, H., Kerrisk, M. E., Vortmeyer, A., Wisniewski, T., Koleske, A. J., Gunther, E. C., Nygaard, H. B., & Strittmatter, S. M.
- Affiliations
- Yale University (US)
- Corresponding author
- Strittmatter, Stephen M.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2013-09
- Volume
- 79
- Issue
- 5
- Pages
- 887-902
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC3768018
- OpenAlex
- W2061342941
- Cited by
- 572
- References
- 65
- Citations by year
- 2026: 28 · 2025: 31 · 2024: 29 · 2023: 35 · 2022: 38 · 2021: 32 · 2020: 59 · 2019: 45 · 2018: 46 · 2017: 63 · 2016: 59 · 2015: 58 · 2014: 45 · 2013: 4
- FWCI
- 34.36
- Type
- journal article
- Language
- en
- Update notices
- erratum (2013-10-16)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute on Aging (P30AG008051, R01AG034924)
- National Institute of General Medical Sciences (T32GM007223, T32GM007205)
- National Institute of Neurological Disorders and Stroke (R01NS074319, R01NS073502, R01NS080388)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- metabotropic glutamate receptor 5, amyloid-beta oligomers, cellular prion protein, Alzheimer's disease, Fyn, postsynaptic density, intracellular calcium signaling, eEF2 phosphorylation, dendritic spine loss, learning and memory impairment, synaptic loss
- MeSH terms
- Alzheimer Disease, Animals, Calcium, Cells, Cultured, Humans, Neurons, Oocytes, Phosphorylation, Xenopus, Signal Transduction, Amyloid beta-Peptides, Receptors, Metabotropic Glutamate, PrPC Proteins, Proto-Oncogene Proteins c-fyn, Mice, Elongation Factor 2 Kinase, HEK293 Cells, Post-Synaptic Density, Receptor, Metabotropic Glutamate 5
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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