Evidence map›Paper›PMID 23690026›Full record

ReviewCurrent neurology and neuroscience reports2013

Vesicular integrity in Parkinson's disease.

Shawn P Alter, Gina M Lenzi, Alison I Bernstein, Gary W Miller

Open access · greenAbstract readReview
In one paragraph

Review in Current neurology and neuroscience reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. [Brain communications · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. DNAJC6 Mutations Disrupt Dopamine Homeostasis in Juvenile Parkinsonism-Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Shawn P AlterDepartment of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
Gina M Lenzi
Alison I Bernstein
Gary W Miller
Emory University · US

Funding

Pilot Project ProgramP30ES019776 · NIEHS · EMORY UNIVERSITY · PI Carmen Joseph Marsit · 2013 to 2026
$22.6M
Graduate and Postdoctoral Training in ToxicologyT32ES012870 · NIEHS · EMORY UNIVERSITY · PI Carmen Joseph Marsit · 2004 to 2026
$9.1M
Udall Parkinson's Disease Center at Emory University: Circuitry to TherapyP50NS071669 · NINDS · EMORY UNIVERSITY · PI WICHMANN, THOMAS · 2010 to 2015
$6.8M
PROJECT 3: METABOLOMIC BIOMARKERS OF PARKINSON'S DISEASEP01ES016731 · NIEHS · EMORY UNIVERSITY · PI MILLER, GARY W · 2008 to 2012
$6.7M
Graduate Training in the Pharmacological StudiesT32GM008602 · NIGMS · EMORY UNIVERSITY · PI HALL, RANDY A. · 1996 to 2021
$5.1M
Training Program in Neurobiology of Drug AbuseT32DA015040 · NIDA · EMORY UNIVERSITY · PI KUHAR, MICHAEL J · 2003 to 2012
$3.6M
NIDA NIH HHS T32 DA015040NIEHS NIH HHS P01 ES016731NIEHS NIH HHS P30 ES019776NIEHS NIH HHS T32 ES012870NIGMS NIH HHS T32 GM008602NINDS NIH HHS P50 NS071669
6 · The paper itself

Abstract

The defining motor characteristics of Parkinson's disease (PD) are mediated by the neurotransmitter dopamine (DA). Dopamine molecules spend most of their lifespan stored in intracellular vesicles awaiting release and very little time in the extracellular space or the cytosol. Without proper packaging of transmitter and trafficking of vesicles to the active zone, dopamine neurotransmission cannot occur. In the cytosol, dopamine is readily oxidized; excessive cytosolic dopamine oxidation may be pathogenic to nigral neurons in PD. Thus, factors that disrupt vesicular function may impair signaling and increase the vulnerability of dopamine neurons. This review outlines the many mechanisms by which disruption of vesicular function may contribute to the pathogenesis of PD. From direct inhibition of dopamine transport into vesicles by pharmacological or toxicological agents to alterations in vesicle trafficking by PD-related gene products, variations in the proper compartmentalization of dopamine can wreak havoc on a functional dopamine pathway. Findings from patient populations, imaging studies, transgenic models, and mechanistic studies will be presented to document the relationship between impaired vesicular function and vulnerability of the nigrostriatal dopamine system. Given the deleterious effects of impaired vesicular function, strategies aimed at enhancing vesicular function may be beneficial in the treatment of PD.

Indexed as

AnimalsBiomarkersDopaminergic NeuronsDopamine Uptake InhibitorsHumansModels, NeurologicalParkinson DiseaseSynaptic VesiclesVesicular Monoamine Transport ProteinsBiomarkersDopamine Uptake InhibitorsVesicular Monoamine Transport Proteins

Identifiers

PMID23690026
PMCPMC4019229
OpenAlexW2013568755

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.