# Tracing inflammasomes in Alzheimer’s: insights from bibliometric analysis

**Authors:** Yingjun Chen, Hui Pei, Hao Li, Wenjun Zeng, Zhitao Li

PMC · DOI: 10.3389/fneur.2025.1540083 · Frontiers in Neurology · 2025-06-05

## TL;DR

This paper uses bibliometric analysis to explore how research on inflammasomes in Alzheimer’s disease has evolved, highlighting key trends and research hotspots.

## Contribution

The study provides a comprehensive bibliometric and knowledge mapping analysis of inflammasome research in Alzheimer’s disease from 2000 to 2024.

## Key findings

- The NLRP3 inflammasome is a major focus in Alzheimer’s research, linked to Aβ and tau proteins.
- China leads in publication quantity, while the U.S. leads in high-quality research output.
- Neuroinflammation and microglia activation are key research themes in the field.

## Abstract

Alzheimer’s disease is one common type of dementia. Numerous studies have suggested a correlation between Alzheimer’s disease and inflammation. The inflammasome is the core of the inflammatory response and plays an important role in the inflammatory response. Currently, ample evidence has shown that inflammasomes are closely related to the occurrence and development of Alzheimer’s disease.

To explore the evolution and development trends of inflammasomes in Alzheimer’s disease using bibliometric and knowledge mapping analysis. By identifying research hotspots and emerging topics, we aim to provide new insights and directions for researchers in this field.

All data related to inflammasomes in Alzheimer’s disease from 2000 to 2024 were collected from the Web of Science Core Collection (WoSCC), and annual publications, national publication trends, and proportion charts were analyzed and plotted using GraphPad price v8.0.2. Additionally, CiteSpace (6.2.4R (64-bit) Advanced Edition), and VOSviewer (version 1.6.18) were used to analyze and visualize these data.

A total of 1,128 publications related to the inflammasome in Alzheimer’s disease were recorded in the WoSCC, comprising 738 articles and 390 reviews. The literature was mainly from 68 countries/regions and 1,545 institutions, particularly China (n = 464) and the USA (n = 266). Despite China’s leading in publication quantity, the United States holds a prominent position in the field due to the higher quality of its scholarly articles. The institution that contributes the most publications is the Helmholtz Association. JOURNAL OF MOLECULAR SCIENCES was a prolific contributor, and Nature was the most frequently cited journal. Keyword analysis showed that nlrp3 inflammasome, neuroinflammation, microglia activation, and amyloid-beta were the most common terms, reflecting the main research interests in currently published papers in this field. Research in this field primarily focuses on the NLRP3 inflammasome, which is closely associated with pathological products like Aβ and tau proteins. It can induce pyroptosis and accelerate the progression of Alzheimer’s disease.

The NLRP3 inflammasome is critical in Alzheimer’s disease (AD) pathogenesis. However, the peak of related literature was in 2023, suggesting a potential decline in this research hotspot. There is an urgent need to explore new pathogenic mechanisms for AD. Clearly, this is an important direction that requires deep thinking and breakthroughs.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548]
- **Proteins:** ab (abrupt), MAPT (microtubule associated protein tau)
- **Diseases:** Alzheimer’s disease (MONDO:0004975)

## Full-text entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}
- **Diseases:** neuroinflammation (MESH:D000090862), AD (MESH:D000544), inflammation (MESH:D007249), dementia (MESH:D003704), JOURNAL OF MOLECULAR SCIENCES (MESH:C567116)

## Full text

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## Figures

16 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12176572/full.md

## References

18 references — full list in the complete paper: https://tomesphere.com/paper/PMC12176572/full.md

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Source: https://tomesphere.com/paper/PMC12176572