# Research trends on neuroinflammation in Parkinson’s disease: an exploratory analysis

**Authors:** Yan-Jun Chen, Ming-Rong Xie, Fang Liu, Sheng-Qiang Zhou, Bo Li

PMC · DOI: 10.3389/fnagi.2026.1699038 · Frontiers in Aging Neuroscience · 2026-02-04

## TL;DR

This paper analyzes trends in Parkinson’s disease neuroinflammation research, identifying key contributors, institutions, and emerging topics like gut microbiota.

## Contribution

A novel bibliometric analysis of neuroinflammation in Parkinson’s disease, highlighting recent research hotspots and influential contributors.

## Key findings

- China leads in publications on PD neuroinflammation, while Norway has the greatest influence.
- Gut microbiota and the brain-gut axis are emerging research hotspots in the field.
- Microglia, oxidative stress, and alpha-synuclein are central themes in current studies.

## Abstract

Neuroinflammation is a core mechanism in the pathogenesis of Parkinson’s disease (PD). Research on PD and neuroinflammation has been steadily increasing. This study aims to explore and analyze the current status, hotspots, and future directions of neuroinflammation-associated research in PD.

Data were retrieved from the Web of Science and PubMed databases. CiteSpace, VOSviewer, and the R package bibliometrix were used for data analysis and visualization.

Publications on neuroinflammation in PD showed an upward trend. China had the most publications, while Norway exhibited the greatest influence. Shanghai Jiao Tong University was the most prolific institution, whereas Arizona State University demonstrated the strongest influence. The International Journal of Molecular Sciences was the most prolific journal in this field, and Cell had the strongest impact. The most productive author was Hong, Jau-Shyong, and the most influential author was Block, Michelle L. High-frequency keywords included PD, neuroinflammation, microglia, oxidative stress, alpha-synuclein, neurodegeneration, inflammation, and mouse models. Gut microbiota has become a recent focus of research.

Over the past two decades, research on neuroinflammation in PD has been continuously increasing. The research hotspots included microglia, oxidative stress, α-synuclein, brain-gut axis, and gut microbiota. This field is developing toward a multi-dimensional and in-depth exploration of mechanisms.

## Linked entities

- **Diseases:** Parkinson’s disease (MONDO:0005180)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513] {aka COII, MTCO2}, MPO (myeloperoxidase) [NCBI Gene 4353], SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, TSPO (translocator protein) [NCBI Gene 706] {aka BPBS, BZRP, DBI, IBP, MBR, PBR}, Snca (synuclein, alpha) [NCBI Gene 20617] {aka NACP, alpha-Syn, alphaSYN}
- **Diseases:** mitochondrial dysfunction (MESH:D028361), PD (MESH:D010300), bradykinesia (MESH:D018476), resting tremor (MESH:D014202), death (MESH:D003643), neurological damage (MESH:D020196), postural instability (MESH:D054972), gastrointestinal symptoms (MESH:D012817), inflammation (MESH:D007249), neurodegeneration (MESH:D019636), of Disease (MESH:D004194), Neuroinflammation (MESH:D000090862), Lewy bodies (MESH:D020961), Huntington's disease (MESH:D006816), neurotoxicity (MESH:D020258), Alzheimer's (MESH:D000544), constipation (MESH:D003248), neurogenic inflammation (MESH:D020078), neuronal damage (MESH:D009410), movement disorders (MESH:D009069), rigidity (MESH:D009127), motor deficits (MESH:D009461)
- **Chemicals:** [11C]PK11195 (MESH:C504060), palmitoylethanolamide (MESH:C005958), DPA713 (MESH:C507091), PBR28 (-), celecoxib (MESH:D000068579), zonisamide (MESH:D000078305), RNS (MESH:D026361), AZD3241 (MESH:C000602652), butyrate (MESH:D002087), minocycline (MESH:D008911), LPS (MESH:D008070), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MESH:D015632), 6-OHDA (MESH:D016627), 11C]PBR28 (MESH:C526315), ROS (MESH:D017382), Paraquat (MESH:D010269), SCFA (MESH:D005232), tryptophan (MESH:D014364), dopamine (MESH:D004298)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12913463/full.md

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12913463/full.md

## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC12913463/full.md

---
Source: https://tomesphere.com/paper/PMC12913463