Evidence map›Paper›PMID 34414447›Full record

ReviewMolecular medicine reports2021

Roles of α‑synuclein in gastrointestinal microbiome dysbiosis‑related Parkinson's disease progression (Review).

Qingchun Lei, Tingting Wu, Jin Wu, Xiaogang Hu, Yingxia Guan, Ying Wang, Jinyuan Yan, Guolin Shi

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Peripheral proteinopathy in neurodegenerative diseases.Translational neurodegeneration · 2025
    Review
  17. Review
  18. Review
  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

8 authors at 3 institutions in 1 country.

Qingchun Lei *Department of Neurosurgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Tingting Wu *Department of Neurosurgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Jin WuDepartment of Neurosurgery, Puer People's Hospital, Pu'er, Yunnan 665000, P.R. China.
Xiaogang HuDepartment of Neurosurgery, Puer People's Hospital, Pu'er, Yunnan 665000, P.R. China.
Yingxia GuanDepartment of Vasculocardiology, The Affiliated Hospital of Yunnan University, Kunming, Yunnan 650021, P.R. China.
Ying WangDepartment of Neurosurgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Jinyuan YanDepartment of Neurosurgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Guolin ShiDepartment of Neurosurgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, P.R. China.
Kunming Medical University · CNPuer University · CNYunnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease amongst the middle‑aged and elderly populations. Several studies have confirmed that the microbiota‑gut‑brain axis (MGBA) serves a key role in the pathogenesis of PD. Changes to the gastrointestinal microbiome (GM) cause misfolding and abnormal aggregation of α‑synuclein (α‑syn) in the intestine. Abnormal α‑syn is not eliminated via physiological mechanisms and is transported into the central nervous system (CNS) via the vagus nerve. The abnormal levels of α‑syn aggregate in the substantia nigra pars compacta, not only leading to the formation of eosinophilic Lewis Bodies in the cytoplasm and mitochondrial dysfunction in dopaminergic (DA) neurons, but also leading to the stimulation of an inflammatory response in the microglia. These pathological changes result in an increase in oxidative stress (OS), which triggers nerve cell apoptosis, a characteristic of PD. This increase in OS further oxidizes and intensifies abnormal aggregation of α‑syn, eventually forming a positive feedback loop. The present review discusses the abnormal accumulation of α‑syn in the intestine caused by the GM changes and the increased levels of α‑syn transport to the CNS via the MGBA, resulting in the loss of DA neurons and an increase in the inflammatory response of microglial cells in the brain of patients with PD. In addition, relevant clinical therapeutic strategies for improving the GM and reducing α‑syn accumulation to relieve the symptoms and progression of PD are described.

Indexed as

Disease ProgressionAgedalpha-SynucleinBacteriaBrainBrain-Gut AxisDopaminergic NeuronsDysbiosisGastrointestinal MicrobiomeHumansMicrogliaMiddle AgedNeurodegenerative DiseasesOxidative StressParkinson Diseasealpha-SynucleinSNCA protein, humangastrointestinal microbiomemicrobiota‑gut‑brain axismicrogliaoxidative stressParkinson's diseaseα‑synuclein

Identifiers

PMID34414447
PMCPMC8404091
OpenAlexW3195983104

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.