Evidence map›Paper›PMID 22941241›Full record

ArticleActa neuropathologica2012

Parkinson's disease is not associated with gastrointestinal myenteric ganglion neuron loss.

Dana M Annerino, Shawn Arshad, Georgia M Taylor, Charles H Adler, Thomas G Beach, James G Greene

Open access · greenAbstract read
In one paragraph

Article in Acta neuropathologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
9.4field-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

97 citing papers in PubMed, 195 citations in OpenAlex.

  1. Trial
  2. Progress of Immunotherapies in Parkinson's Disease.CNS neuroscience & therapeutics · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. The interrelationship between intestinal immune cells and enteric α-synuclein in the progression of Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  8. Review
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Review
  15. Gastrointestinal dysmotility in rodent models of Parkinson's disease.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

37 more citing papers are in PubMed but not listed here.

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

6 authors at 4 institutions in 1 country.

Dana M AnnerinoDepartment of Neurology, Emory University School of Medicine, Atlanta, GA 30322, USA.
Shawn Arshad
Georgia M Taylor
Charles H Adler
Thomas G Beach
James G Greene
Emory University · USBanner Sun Health Research Institute · USMayo Clinic in Arizona · USWoodruff Health Sciences Center · US

Funding

Research Education ComponentP30AG019610 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI ALEXANDER, GENE E · 2001 to 2020
$32.5M
Molecular mechanism of selective neuronal vulnerabilityK08NS048858 · NINDS · EMORY UNIVERSITY · PI GREENE, JAMES G · 2005 to 2009
$837k
NIA NIH HHS P30 AG019610NIA NIH HHS P30 AG19610NINDS NIH HHS K08 NS048858
6 · The paper itself

Abstract

Gastrointestinal dysfunction is a prominent non-motor feature of Parkinson's disease (PD) that contributes directly to the morbidity of patients, complicates management of motor symptoms, and may herald incipient PD in patients without motor disability. Although PD has traditionally been considered a disease of dopaminergic neurons in the substantia nigra, analyses of gastrointestinal samples from PD patients have consistently revealed pathology in the enteric nervous system. The relationship of PD pathology to GI dysmotility is poorly understood, and this lack of understanding has led to limited success in developing treatments for PD-related GI symptoms. We have quantitatively compared myenteric neuron density and relative abundance of NO, VIP, and catecholamine neurons between patients with PD and control individuals along the length of the GI tract. In addition, we have examined the frequency of GI α-synuclein neuritic pathology and its co-localization with the same neuronal markers. We have included a comparison with a small population of patients with incidental Lewy bodies found at autopsy. These data indicate that there is no neuronal loss in the myenteric plexus in PD. Lewy body pathology parallels parasympathetic autonomic input from the dorsal motor nucleus of the vagus, not the distribution of extrinsic sympathetic input or intrinsic enteric neurons, and is only rarely co-localized with tyrosine hydroxylase. These data provide a critical background to which further analyses of the effect of PD on the GI tract may be compared and suggest that neuropathology in myenteric neurons is unlikely to be a causative factor in PD-related GI dysmotility.

Indexed as

AgedAged, 80 and overalpha-SynucleinCatecholaminesCell CountELAV ProteinsEnteric Nervous SystemFemaleHumansLewy BodiesMaleMyenteric PlexusNerve Tissue ProteinsNeuronsNitric Oxide Synthase Type IParkinson Diseasealpha-SynucleinCatecholaminesELAV ProteinsNerve Tissue ProteinsNitric Oxide Synthase Type ITyrosine 3-MonooxygenaseVasoactive Intestinal Peptide

Identifiers

PMID22941241
PMCPMC3473167
OpenAlexW1999950065

What OpenQuestion holds

Textmetadata
LicenceTDM
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.