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Dysfunction of NMDA receptors in Alzheimer’s disease
Open accessAbstract
N-methyl-D-aspartate receptors (NMDARs) play a pivotal role in the synaptic transmission and synaptic plasticity thought to underlie learning and memory. NMDARs activation has been recently implicated in Alzheimer's disease (AD) related to synaptic dysfunction. Synaptic NMDARs are neuroprotective, whereas overactivation of NMDARs located outside of the synapse cause loss of mitochondrial membrane potential and cell death. NMDARs dysfunction in the glutamatergic tripartite synapse, comprising presynaptic and postsynaptic neurons and glial cells, is directly involved in AD. This review discusses that both beta-amyloid (Aβ) and tau perturb synaptic functioning of the tripartite synapse, including alterations in glutamate release, astrocytic uptake, and receptor signaling. Particular emphasis is given to the role of NMDARs as a possible convergence point for Aβ and tau toxicity and possible reversible stages of the AD through preventive and/or disease-modifying therapeutic strategies.
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![Fig. 1 Structure and domain organization of NMDA receptors. Linear representation of the subunit polypeptide chain and schematic illustration of the subunit topology. NMDARs subunits have a modular structure composed of two extracellular domains [the ATD (green) and the LBD (yellow)]; a TMD (cyan) that forms part of the ion channel pore; and an intracellular CTD. The LBD is defined by two segments of amino acids termed S1 and S2. The TMD contains three membrane-spanning helices (M1, M3, and M4) and a membrane re-entrant loop (M2)](/paper-figures/5a9f61267ae6405486f516579de77eb5/dysfunction-of-nmda-receptors-in-alzheimers-disease-figure-1.jpg)
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“The relevance of NMDAR in AD lends support from studies showing that partial blockade of NMDAR overstimulation with NMDAR antagonists rescues Aβ-induced LTP impairment and cognitive function in various animal models [69].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [69]
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“Lastly, both Aβ and τ perturb PSD-95-anchored com - plexes, impairing NMDAR and AMPAR trafficking and sig - naling, amplifying oxidative stress and synaptic failure (Liu et al. 2019; Zhang et al. 2016; Tu et al. 2014).”
Proteomics Reveals Blood−Brain Barrier Membrane Protein Remodeling in Amyloid-β Pathology
Hyvärinen, J., Todorovska, R., Palacios, M. D. P., Gynther, M., Afonin, A., Lehtonen, M., Auriola, S., Saveleva, L., Kanninen, K. M., Fricker, G., et al. (2026) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.6c00935
Metadata
- Authors
- Zhang, Y., Li, P., Feng, J., & Wu, M.
- Affiliations
- Central South University (CN)
- Corresponding author
- Wu, Minghua
- Venue
- Neurological Sciences
- Published
- 2016-03-12
- Volume
- 37
- Issue
- 7
- Pages
- 1039-1047
- ISSN
- 1590-1874 (ISSN-L)
- 1590-3478
- PMC
- PMC4917574
- OpenAlex
- W2293608890
- Cited by
- 282
- References
- 72
- Citations by year
- 2026: 15 · 2025: 30 · 2024: 36 · 2023: 29 · 2022: 29 · 2021: 27 · 2020: 39 · 2019: 23 · 2018: 35 · 2017: 15 · 2016: 3
- FWCI
- 2.97
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Neurological Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- 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
- NMDA receptor, Alzheimer's disease, synaptic dysfunction, tripartite synapse, amyloid-beta, tau protein, glutamate release, astrocytes, synaptic plasticity, mitochondrial membrane potential, neuroprotection, disease-modifying therapy
- MeSH terms
- Alzheimer Disease, Humans, Synapses, Receptors, N-Methyl-D-Aspartate, Amyloid beta-Peptides, tau Proteins
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