Evidence map›Paper›PMID 37066923›Full record

ReviewJournal of Parkinson's disease2023

Immunological Features of LRRK2 Function and Its Role in the Gut-Brain Axis Governing Parkinson's Disease.

Inga Peter, Warren Strober

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of Parkinson's disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Nutrition as a systems regulator of brain aging trajectories.Frontiers in molecular neuroscience · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Multiple sclerosis inFrontiers in neurology · 2024
    Article
  12. 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 2 institutions in 1 country.

Inga PeterDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Warren StroberMucosal Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Icahn School of Medicine at Mount Sinai · USNational Institutes of Health · US

Funding

Regulation Of Immune Responses In Humans and in Experimental AnimalsZIAAI000432 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$11.3M
Immunoregulatory Defects In Inflammatory Bowel DiseaseZIAAI000354 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$8.7M
Molecular and Cellular Basis of the Gut-Brain Axis in Parkinsons DiseaseP20NS123220 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI YUE, ZHENYU · 2021 to 2022
$1.0M
NINDS NIH HHS P20 NS123220
6 · The paper itself

Abstract

Emerging evidence implicates intestinal involvement in the onset and/or progression on the selective degeneration of dopaminergic neurons characterizing Parkinson's disease (PD). On the one hand, there are studies supporting the Braak hypothesis that holds that pathologic α-synuclein, a hallmark of PD, is secreted by enteric nerves into intestinal tissue and finds its way to the central nervous system (CNS) via retrograde movement in the vagus nerve. On the other hand, there is data showing that cells bearing leucine-rich repeat kinase 2 (LRRK2), a signaling molecule with genetic variants associated with both PD and with inflammatory bowel disease, can be activated in intestinal tissue and contribute locally to intestinal inflammation, or peripherally to PD pathogenesis via cell trafficking to the CNS. Importantly, these gut-centered factors affecting PD development are not necessarily independent of one another: they may interact and enhance their respective pathologic functions. In this review, we discuss this possibility by analysis of studies conducted in recent years focusing on the ability of LRRK2 to shape immunologic responses and the role of α-synuclein in influencing this ability.

Indexed as

alpha-SynucleinParkinson DiseaseBrain-Gut AxisDopaminergic NeuronsHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Signal Transductionalpha-SynucleinLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanenteric nervous systemGut-brain axisintestinal inflammationLRRK2Parkinson’s diseaseα-synuclein

Identifiers

PMID37066923
PMCPMC10200211
OpenAlexW4364361142

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.