# The role of ionotropic glutamate receptors in Alzheimer's disease: A scientometric analysis

**Authors:** Yunsheng Liu, Rongde Zhong, Qian Li, Yuyan Wang, Jinfang Zhang, Zengwei Kou

PMC · DOI: 10.1177/13872877261423577 · Journal of Alzheimer's Disease · 2026-03-03

## TL;DR

This paper analyzes global research trends on ionotropic glutamate receptors in Alzheimer's disease, highlighting their role in disease mechanisms and potential therapies.

## Contribution

A comprehensive bibliometric analysis of iGluR research in Alzheimer's disease from 1986 to 2025, identifying trends and future directions.

## Key findings

- Research on NMDA receptors has shifted from basic mechanisms to clinical applications like memantine therapy.
- Emerging trends focus on AMPA and kainate receptors, with growing contributions from Chinese researchers.
- Future research should prioritize understudied iGluR subtypes and leverage new technologies like AI and single-cell sequencing.

## Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β plaques, neurofibrillary tangles, and synaptic dysfunction. Dysregulation of ionotropic glutamate receptors (iGluRs), including NMDA, AMPA, and kainate receptors, contributes to excitotoxicity, synaptic impairment, and cognitive decline, underscoring their therapeutic potential.

This study aimed to conduct a comprehensive bibliometric analysis of iGluR research in AD from January 1, 1986 to August 23, 2025.

We systematically searched and analyzed the publications related to iGluRs in AD from PubMed, Web of Science, and Scopus using CiteSpace, VOSviewer, and Bibliometrix. Metrics included publication volume, citation impact, international collaborations, keyword co-occurrence, and burst detection.

A total of 4810 papers were identified for analysis. The most prolific country, institution, journal, and author were the United States, Harvard University system, Journal of Neurochemistry, and Lipton SA, respectively. Research has evolved from NMDAR dysfunction and Aβ toxicity to clinical applications, such as memantine therapy, with recent trends focusing on AMPAR modulation and neuroprotection. Emerging researchers from China have demonstrated rapid growth. Keyword analysis reflected a sustained interest in molecular mechanisms and an increasing emphasis on clinical translation.

This study delineates the evolution of iGluR research in AD from mechanistic insights to therapeutic innovation. While NMDARs remain central, future efforts should prioritize understudied targets like AMPARs and KARs, and leverage emerging technologies, such as cryo-electron microscopy, single-cell sequencing, and artificial intelligence, to refine therapeutic strategies and facilitate personalized medicine. It highlights targeted iGluR modulation as a promising therapeutic avenue for combating AD.

Graphical AbstractThis is a visual representation of the abstract.

This is a visual representation of the abstract.

## Linked entities

- **Proteins:** Nmdar1 (NMDA receptor 1), ampA (adhesion modulation protein A)
- **Chemicals:** memantine (PubChem CID 4054)
- **Diseases:** Alzheimer's disease (MONDO:0004975)

## Full-text entities

- **Genes:** KARS1 (lysyl-tRNA synthetase 1) [NCBI Gene 3735] {aka CMTRIB, DEAPLE, DFNB89, KARS, KARS2, KRS}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}
- **Diseases:** synaptic dysfunction (MESH:C536122), cognitive decline (MESH:D003072), toxicity (MESH:D064420), synaptic impairment (MESH:D012183), neurofibrillary tangles (MESH:D055956), neurodegenerative disorder (MESH:D019636), 's disease (MESH:D004194), NMDAR dysfunction (MESH:D060426), AD (MESH:D000544)
- **Chemicals:** memantine (MESH:D008559)

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13022013/full.md

## References

42 references — full list in the complete paper: https://tomesphere.com/paper/PMC13022013/full.md

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Source: https://tomesphere.com/paper/PMC13022013