The DOI matches its Crossref record; 54 of the 55 references it cites were found in a registry or an index.
Biochemical and molecular studies of NMDA receptor subunits NR1/2A/2B in hippocampal subregions throughout progression of Alzheimer's disease pathology
Open accessAbstract
Alzheimer's disease (AD) is characterized by loss of specific cell populations within selective subregions of the hippocampus. Excitotoxicity, mediated via ionotropic glutamate receptors, may play a crucial role in this selective neuronal vulnerability. We investigated whether alterations in NMDA receptor subunits occurred during AD progression. Employing biochemical and in situ hybridization techniques in subjects with a broad range of AD pathology, protein levels, and mRNA expression of NR1/2A/2B subunits were assayed. With increasing AD neuropathology, protein levels and mRNA expression for NR1/2B subunits were significantly reduced, while the NR2A subunit mRNA expression and protein levels were unchanged. Cellular analysis of neuronal mRNA expression revealed a significant increase in the NR2A subunit in subjects with moderate neurofibrillary tangle neuropathology. This investigation supports the hypothesis that alterations occur in the expression of specific NMDA receptor subunits with increasing AD pathologic severity, which is hypothesized to contribute to the vulnerability of these neurons.
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“GluN2A and GluN2B expression levels (mRNA and protein) were also found to decrease in vulnerable brain regions, including the hippocampus and cerebral cortex in AD [62].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [62]
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Cites
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
Heteromeric NMDA receptors: molecular and functional distinction of subtypes
Monyer, H., Sprengel, R., Schoepfer, R., Herb, A., Higuchi, M., Lomeli, H., Burnashev, N., Sakmann, B., & Seeburg, P. H. (1992) · Science · doi:10.1126/science.256.5060.1217 · Cited by 2,541
Alzheimer's disease: cell-specific pathology isolates the hippocampal formation.
Hyman, B. T., Van Hoesen, G. W., Damasio, A. R., & Barnes, C. L. (1984) · Science · doi:10.1126/science.6474172 · Cited by 2,268
Neurotrophic and Neurotoxic Effects of Amyloid β Protein: Reversal by Tachykinin Neuropeptides
Yankner, B. A., Duffy, L. K., & Kirschner, D. A. (1990) · Science · doi:10.1126/science.2218531 · Cited by 1,975
The physiology of excitatory amino acids in the vertebrate central nervous system
Mayer, M. L., & Westbrook, G. L. (1987) · Progress in Neurobiology · doi:10.1016/0301-0082(87)90011-6 · Cited by 1,711
Mattson, M. P., Cheng, B., Davis, D. G., Bryant, K., Lieberburg, I. M., & Rydel, R. E. (1992) · Journal of Neuroscience · doi:10.1523/jneurosci.12-02-00376.1992 · Cited by 1,633
Molecular diversity of the NMDA receptor channel
Kutsuwada, T., Kashiwabuchi, N., Mori, H., Sakimura, K., Kushiya, E., Araki, K., Meguro, H., Hisashi, M., Kumanishi, T., Arakawa, M., et al. (1992) · Nature · doi:10.1038/358036a0 · Cited by 1,352
Molecular characterization of the family of the N-methyl-D-aspartate receptor subunits.
Ishii, T. M., Moriyoshi, K., Sugihara, H., Sakurada, K., Kadotani, H., Yokoi, M., Akazawa, C., Shigemoto, R., Mizuno, N., & Masu, M. (1993) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)53849-7 · Cited by 980
N-methyl-D-aspartic acid receptor structure and function
McBain, C. J., & Mayer, M. L. (1994) · Physiological Reviews · doi:10.1152/physrev.1994.74.3.723 · Cited by 976
Neurotoxicity of a Fragment of the Amyloid Precursor Associated with Alzheimer's Disease
Yankner, B. A., Dawes, L. R., Fisher, S., Villa-Komaroff, L., Oster-Granite, M. L., & Neve, R. L. (1989) · Science · doi:10.1126/science.2474201 · Cited by 907
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Lacor, P. N., Buniel, M. C., Furlow, P. W., Sanz Clemente, A., Velasco, P. T., Wood, M., Viola, K. L., & Klein, W. L. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.3501-06.2007 · Cited by 1,188
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00391-7 · Cited by 994
Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease
Bezprozvanny, I., & Mattson, M. P. (2008) · Trends in Neurosciences · doi:10.1016/j.tins.2008.06.005 · Cited by 938
Selective vulnerability in neurodegenerative diseases
Fu, H., Hardy, J., & Duff, K. E. (2018) · Nature Neuroscience · doi:10.1038/s41593-018-0221-2 · Cited by 585
The Role of NMDA Receptors in Alzheimer’s Disease
Liu, J., Chang, L., Song, Y., Li, H., & Wu, Y. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00043 · Cited by 535
Metadata
- Authors
- Mishizen-Eberz, A. J., Rissman, R. A., Carter, T. L., Ikonomovic, M. D., Wolfe, B. B., & Armstrong, D. M.
- Affiliations
- Lankenau Institute for Medical Research (US)
- Georgetown University Medical Center (US)
- Corresponding author
- Mishizen-Eberz, Amanda J
- ORCID
- Rissman, Robert A
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2004-02
- Volume
- 15
- Issue
- 1
- Pages
- 80-92
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2024849224
- Cited by
- 156
- References
- 55
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 9 · 2021: 7 · 2020: 5 · 2019: 5 · 2018: 6 · 2017: 7 · 2016: 10 · 2015: 8 · 2014: 12 · 2013: 7 · 2012: 6
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (5r01ag008206-15)
- National Institute on Aging (AG 08206)
- 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
- Alzheimer's disease, NMDA receptor subunits, NR1, NR2A, NR2B, hippocampus, excitotoxicity, ionotropic glutamate receptors, neurofibrillary tangles, selective neuronal vulnerability, mRNA expression, protein abundance, disease progression
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Female, Hippocampus, Humans, Immunohistochemistry, Male, Middle Aged, Neurons, RNA, Messenger, Down-Regulation, Up-Regulation, Receptors, N-Methyl-D-Aspartate, Neurofibrillary Tangles, Disease Progression, Protein Subunits
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