Evidence map›Paper›PMID 35897024›Full record

ReviewJournal of biomedical science2022

Gut microenvironmental changes as a potential trigger in Parkinson's disease through the gut-brain axis.

Szu-Ju Chen, Chin-Hsien Lin

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
8.3field-weighted citation impact, top 2% of its field
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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

38 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Gut-Brain Signaling in Parkinson's Disease: A Narrative Review.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Management of Gastrointestinal Symptoms in Parkinson's Disease.Journal of central nervous system disease · 2025
    Review
  16. Review
  17. Article
  18. Impaired gut barrier integrity and reduced colonic expression of free fatty acid receptors in patients with Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

Szu-Ju ChenDepartment of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, 100, Taiwan.
Chin-Hsien LinDepartment of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, 100, Taiwan. chlin@ntu.edu.tw.ORCID http://orcid.org/0000-0001-8566-7573
National Taiwan University · TW

Funding

Ministry of Science and Technology, Taiwan MOST 109-2320-B-002-073 -National Health Research Institutes NHRI-EX111-11136NINational Taiwan University NTU-110-A-CC-5400-64841
6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease attributed to the synergistic effects of genetic risk and environmental stimuli. Although PD is characterized by motor dysfunction resulting from intraneuronal alpha-synuclein accumulations, termed Lewy bodies, and dopaminergic neuronal degeneration in the substantia nigra, multiple systems are involved in the disease process, resulting in heterogenous clinical presentation and progression. Genetic predisposition to PD regarding aberrant immune responses, abnormal protein aggregation, autophagolysosomal impairment, and mitochondrial dysfunction leads to vulnerable neurons that are sensitive to environmental triggers and, together, result in neuronal degeneration. Neuropathology studies have shown that, at least in some patients, Lewy bodies start from the enteric nervous system and then spread to the central dopaminergic neurons through the gut-brain axis, suggesting the contribution of an altered gut microenvironment in the pathogenesis of PD. A plethora of evidence has revealed different gut microbiomes and gut metabolites in patients with PD compared to unaffected controls. Chronic gut inflammation and impaired intestinal barrier integrity have been observed in human PD patients and mouse models of PD. These observations led to the hypothesis that an altered gut microenvironment is a potential trigger of the PD process in a genetically susceptible host. In this review, we will discuss the complex interplay between genetic factors and gut microenvironmental changes contributing to PD pathogenesis.

Indexed as

Enteric Nervous SystemNeurodegenerative DiseasesParkinson DiseaseAnimalsBrain-Gut AxisDopaminergic NeuronsHumansInflammationMiceGastrointestinal inflammationGut–brain axisGut microbiotaGut microenvironmentImpaired intestinal barrierParkinson’s disease

Identifiers

PMID35897024
PMCPMC9327249
OpenAlexW4288723506

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.