The DOI matches its Crossref record; 260 of the 260 references it cites were found in a registry or an index.
Alzheimer's disease, β‐amyloid, glutamate, NMDA receptors and memantine – searching for the connections
Open accessAbstract
β‐amyloid (Aβ) is widely accepted to be one of the major pathomechanisms underlying Alzheimer's disease (AD), although there is presently lively debate regarding the relative roles of particular species/forms of this peptide. Most recent evidence indicates that soluble oligomers rather than plaques are the major cause of synaptic dysfunction and ultimately neurodegeneration. Soluble oligomeric Aβ has been shown to interact with several proteins, for example glutamatergic receptors of the NMDA type and proteins responsible for maintaining glutamate homeostasis such as uptake and release. As NMDA receptors are critically involved in neuronal plasticity including learning and memory, we felt that it would be valuable to provide an up to date review of the evidence connecting Aβ to these receptors and related neuronal plasticity. Strong support for the clinical relevance of such interactions is provided by the NMDA receptor antagonist memantine. This substance is the only NMDA receptor antagonist used clinically in the treatment of AD and therefore offers an excellent tool to facilitate translational extrapolations from in vitro studies through in vivo animal experiments to its ultimate clinical utility.
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“previous studies showing that A β deposition contributes to disturbed glutamatergic neurotransmission”
From Genetic variants of phospholipase C-γ2 alter the phenotype and function of microglia and confer differential risk for Alzheimer’s disease (2023) · cites this paper as [38]
Experimental — accuracy not yet measuredIn the citing paper
“oAβ has been reported to impair NMDAR-dependent synaptic LTP within hippocampal CA1 and dentate gyrus regions [65].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [65]
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
Lesné, S., Koh, M. T., Kotilinek, L., Kayed, R., Glabe, C. G., Yang, A., Gallagher, M., & Ashe, K. H. (2006) · Nature · doi:10.1038/nature04533 · Cited by 2,769 · cited 2×
“Such amyloid plaques are insoluble, quasicrystalline deposits (Lesne et al., 2006), the main component of which is Ab – a peptide (most commonly 40–42 amino acids in length) that is formed by enzymatic cleavage of the transmembrane amyloid precursor protein (APP) (Hardy and Higgins, 1992; Citron,…”
BackgroundRetractedAlzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Walsh, D. M., Klyubin, I., Fadeeva, J. V., Cullen, W. K., Anwyl, R., Wolfe, M. S., Rowan, M. J., & Selkoe, D. J. (2002) · Nature · doi:10.1038/416535a · Cited by 4,291
Danbolt, N. C. (2001) · Progress in Neurobiology · doi:10.1016/s0301-0082(00)00067-8 · Cited by 4,227
Magnesium gates glutamate-activated channels in mouse central neurones
Nowak, L. M., Bregestovski, P. D., Ascher, P., Herbet, A., & Prochiantz, A. (1984) · Nature · doi:10.1038/307462a0 · Cited by 4,116
Shankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
Diffusible, nonfibrillar ligands derived from Aβ 1–42 are potent central nervous system neurotoxins
Lambert, M. P., Barlow, A. K., Chromy, B. A., Edwards, C., Freed, R., Liosatos, M., Morgan, T. E., Rozovsky, I., Trommer, B., Viola, K. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.11.6448 · Cited by 3,506
Excitatory Amino Acid Transmitters
Watkins, J. C., & Evans, R. H. (1981) · The Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pa.21.040181.001121 · Cited by 2,497
Memantine in Moderate-to-Severe Alzheimer's Disease
Reisberg, B., Doody, R., Stöffler, A., Schmitt, F., Ferris, S., & Möbius, H. J. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa013128 · Cited by 2,043
Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways
Hardingham, G. E., Fukunaga, Y., & Bading, H. (2002) · Nature Neuroscience · doi:10.1038/nn835 · Cited by 1,686
Research works printed but not linked: 3
- Danysz W, 1995, Glutamate in CNS disorders – a revived target for drug development, Drug News Perspect, 8, 261
- Von Euler G, 2008, Soluble Aβ42 oligomers do not cause synaptic degeneration through direct binding to NMDA receptor sites for glutamate, glycine, and non‐competitive blockers, Society for Neuroscience Abstracts, 34, #829.07
- 10.1042/BST0331087 · DOI
Cited by
Sorted by citations
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
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
Sasannejad, C., Ely, E. W., & Lahiri, S. (2019) · Critical Care · doi:10.1186/s13054-019-2626-z · Cited by 326
Dendritic Tau in Alzheimer’s Disease
Ittner, A., & Ittner, L. M. (2018) · Neuron · doi:10.1016/j.neuron.2018.06.003 · Cited by 278
NMDA receptors and memory encoding
Morris, R. G. M. (2013) · Neuropharmacology · doi:10.1016/j.neuropharm.2013.04.014 · Cited by 295
Metadata
- Authors
- Danysz, W., & Parsons, C. G.
- Affiliations
- Merz (Germany) (DE)
- Corresponding author
- Parsons, Chris G
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2012-08-22
- Volume
- 167
- Issue
- 2
- Pages
- 324-352
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC3481041
- OpenAlex
- W1561114541
- Cited by
- 500
- References
- 260
- Citations by year
- 2026: 15 · 2025: 31 · 2024: 38 · 2023: 34 · 2022: 41 · 2021: 35 · 2020: 28 · 2019: 37 · 2018: 45 · 2017: 60 · 2016: 48 · 2015: 33 · 2014: 35 · 2013: 17 · 2012: 2
- FWCI
- 2.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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, amyloid-beta, NMDA receptor, glutamate, glutamate homeostasis, synaptic dysfunction, neurodegeneration, neuroplasticity, learning and memory, memantine, NMDA receptor antagonists, amyloid plaques
- MeSH terms
- Alzheimer Disease, Humans, Memantine, Dopamine Agents, Receptors, N-Methyl-D-Aspartate, Amyloid beta-Peptides, Glutamic Acid
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