Evidence map›Paper›PMID 22719003›Full record

ArticleBrain : a journal of neurology2012

Alterations in axonal transport motor proteins in sporadic and experimental Parkinson's disease.

Yaping Chu, Gerardo A Morfini, Lori B Langhamer, Yinzhen He, Scott T Brady, Jeffrey H Kordower

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed, 1 pooled it
13.3field-weighted citation impact, top 1% 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

171 citing papers in PubMed, 1 synthesis or guideline pooled it, 312 citations in OpenAlex.

  1. Pooled it
  2. Spatiotemporal Progression Patterns of Striatal Dopamine Depletion and Cerebral Hypoperfusion in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  3. Article
  4. Clinical GDNF delivery methods for Parkinson's disease.Journal of Parkinson's disease · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. MicroRNAs and synaptic dysfunction in Parkinson's disease.Molecular therapy. Nucleic acids · 2025
    Review
  13. Review
  14. Article
  15. The mechanochemical cycle of reactive full-length human dynein 1.Nature structural & molecular biology · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Levodopa treatment: impacts and mechanisms throughout Parkinson's disease progression.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  20. Review

111 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 2 institutions in 1 country.

Yaping ChuDepartment of Neurological Sciences, Rush University Medical Centre, 1735 West Harrison Street, Chicago, IL 60612, USA.
Gerardo A Morfini
Lori B Langhamer
Yinzhen He
Scott T Brady
Jeffrey H Kordower
Rush University Medical Center · USUniversity of Illinois Chicago · US

Funding

MOLECULAR MECHANISMS OF AXONAL TRANSPORTR01NS023868 · NINDS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI BRADY, SCOTT THOMAS · 1986 to 2010
$3.7M
NINDS NIH HHS R01 NS023868
6 · The paper itself

Abstract

The progressive loss of the nigrostriatal pathway is a distinguishing feature of Parkinson's disease. As terminal field loss seems to precede cell body loss, we tested whether alterations of axonal transport motor proteins would be early features in Parkinson's disease. There was a decline in axonal transport motor proteins in sporadic Parkinson's disease that preceded other well-known nigral cell-related pathology such as phenotypic downregulation of dopamine. Reductions in conventional kinesin levels precede the alterations in dopaminergic phenotypic markers (tyrosine hydroxylase) in the early stages of Parkinson's disease. This reduction was significantly greater in nigral neurons containing α-synuclein inclusions. Unlike conventional kinesin, reductions in the levels of the cytoplasmic dynein light chain Tctex type 3 subunit were only observed at late Parkinson's disease stages. Reductions in levels of conventional kinesin and cytoplasmic dynein subunits were recapitulated in a rat genetic Parkinson's disease model based on over-expression of human mutant α-synuclein (A30P). Together, our data suggest that α-synuclein aggregation is a key feature associated with reductions of axonal transport motor proteins in Parkinson's disease and support the hypothesis that dopaminergic neurodegeneration following a 'dying-back' pattern involving axonal transport disruption.

Indexed as

AgedAged, 80 and overalpha-SynucleinAnimalsAxonal TransportCase-Control StudiesCytoplasmic DyneinsDopaminergic NeuronsDyneinsFemaleHumansKinesinsMaleMiddle AgedParkinsonian DisordersRatsalpha-SynucleinCytoplasmic DyneinsDyneinsDYNLT3 protein, mouseKinesinsTyrosine 3-Monooxygenase

Identifiers

PMID22719003
PMCPMC4571141
OpenAlexW2106179404

What OpenQuestion holds

Textmetadata
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.