Evidence map›Paper›PMID 41448457›Full record

ArticleJournal of advanced research2026

Parabacteroides goldsteinii mitigates parkinsonism in LRRK2 mutant mice by reducing neuroinflammation through Gut-Brain axis.

Jian-Da Lin, Hsun Li, Chia-Lang Hsu, Tzu-Lung Lin, Hsiao-Li Chuang, Han-I Lin, En-Peng Ho, Yi-Hsuan Chen, Chia-Wei Liu, Ya-Ting Chuang and 8 more

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Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Jian-Da LinDepartment of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan.
Hsun LiDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Chia-Lang HsuDepartment of Medical Research, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan; Graduate Institute of Medical Genomics and Proteomics, National Taiwan University, Taipei, Taiwan; Center for Computational and Systems Biology, National Taiwan University, Taipei, Taiwan.
Tzu-Lung LinDepartment of Medical Biotechnology and Laboratory Science, and Emerging Viral Infections Research Center, Chang Gung University, Taoyuan, Taiwan.
Hsiao-Li ChuangNational Applied Research Laboratories, National Laboratory Animal Center, Taipei, Taiwan.
Han-I LinDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
En-Peng HoDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Yi-Hsuan ChenDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Chia-Wei LiuDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Ya-Ting ChuangDepartment of Medical Research, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yun-Yi LungDepartment of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan.
Chia-Jung LienDepartment of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan.
Huan-Yun ChenDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Wei-Kai WuDepartment of Medical Research, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan; Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ming-Shiang WuDivision of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chia-Chen LuDepartment of Respiratory Therapy, Fu Jen Catholic University, New Taipei City, Taiwan.
Hsin-Chih LaiDepartment of Medical Biotechnology and Laboratory Science, and Emerging Viral Infections Research Center, Chang Gung University, Taoyuan, Taiwan. Electronic address: hsin.lai@revivebio.com.tw.
Chin-Hsien LinDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan; Graduate Institute of Molecular Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; Graduate Institute of Biomedical Engineering, College of Medical Science and Technology, National Taiwan University, Taipei, Taiwan; Graduate Institute of Brain and Mind Sciences, College of Medicine, National Taiwan University, Taipei, Taiwan. Electronic address: chlin@ntu.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlterations in the gut microbiota accompanied by intestinal inflammation are early features of Parkinson's disease (PD). Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene represent a common genetic risk factor for PD and inflammatory bowel disease. Parabacteroides goldsteinii has been reported to alleviate intestinal and systemic inflammation. However, whether modulation of the gut microenvironment at early disease stage can attenuate PD progression remains unclear.

objectiveTo investigate the impact of P. goldsteinii colonization prior to the onset of motor dysfunction on PD progression.

methodsWe established a germ-free PD mouse model carrying the LRRK2 G2019S mutation and administered P. goldsteinii orally at the pre-symptomatic stage to evaluate its effects on motor performance and PD-related neuropathology. Spatial and bulk RNA transcriptomic analyses of brain tissue, together with cytokine profiling, were conducted to assess central changes. To investigate gut immunomodulatory mechanisms, we performed intestinal bulk and single-cell RNA sequencing, spectral flow cytometry as well as cellular bioenergetic analyses.

resultsGerm-free conditions partially alleviated PD-like phenotypes in LRRK2 G2019S mice. Colonization with P. goldsteinii at 5-months of age, prior to motor symptom onset, further improved locomotor performance, reduced neuronal α-synuclein aggregations, and mitigated microglial activation and dopaminergic neurodegeneration. Neuroprotection was mediated through enhanced noncanonical neuronal IL-12 receptor-dependent neurotrophic support without activating the canonical STAT4 phosphorylation pathway, along with suppression of microglial activation and downregulation of LRRK2 kinase activity. At the intestinal level, P. goldsteinii suppressed TLR4-driven inflammation, expanded anti-inflammatory intraepithelial CD4

conclusionP. goldsteinii colonization attenuates the progression of LRRK2-associated parkinsonism by restoring intestinal homeostasis and reducing neuroinflammation. These findings underscore the therapeutic potential of modulating the gut-immune-brain axis during the prodromal stage of PD.

Indexed as

Brain-Gut AxisLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Neuroinflammatory DiseasesParkinson DiseaseParkinsonian DisordersAnimalsBrainDisease Models, AnimalGastrointestinal MicrobiomeMaleMiceMice, Inbred C57BLMutationLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Lrrk2 protein, mouseGut-brain axisGut microbiotaLeucine rich repeat kinase 2Parabacteroides goldsteiniiParkinson’s disease

Identifiers

PMID41448457
PMCPMC13539244

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.