Evidence map›Paper›PMID 20696316›Full record

ArticleProgress in brain research2010

Intracellular signalling pathways in dopamine cell death and axonal degeneration.

Robert E Burke

Abstract read
In one paragraph

Article in Progress in brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
11.7field-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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Dopamine Activates the D1R-ZnCellular and molecular neurobiology · 2023
    Article
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  3. Review
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
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  11. Article
  12. Programmed cell death in Parkinson's disease.Cold Spring Harbor perspectives in medicine · 2012
    Review
  13. 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

1 author at 1 institution in 1 country.

Robert E BurkeDepartment of Neurology, Columbia University, New York, NY, USA. rb43@columbia.edu
Columbia University · US

Funding

TRANSLATIONAL APPROACHES TO NEUROPROTECTION OF AXONS IN PDrP50NS038370 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 1999 to 2014
$24.0M
APOPTOSIS IN SUBSTANTIA NIGRA FOLLOWING STRIATAL INJURYR01NS026836 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 1994 to 2010
$4.3M
Apoptosis in substantia nigraR56NS026836 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BURKE, ROBERT E · 2011 to 2011
$559k
EFFECT OF PERINATAL ASPHYXIA ON STRIATUMR29NS026836 · NINDS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI BURKE, ROBERT E · 1989 to 1993
–
NINDS NIH HHS NS26836NINDS NIH HHS NS38370NINDS NIH HHS P50 NS038370NINDS NIH HHS R01 NS026836NINDS NIH HHS R56 NS026836
6 · The paper itself

Abstract

The pathways of programmed cell death (PCD) are now understood in extraordinary detail at the molecular level. Although much evidence suggests that they are likely to play a role in Parkinson's disease (PD), the precise nature of that role remains unknown. Two pathways of cell death that are especially well characterized are cyclin-dependent kinase 5-mediated phosphorylation of myocyte enhancer factor 2 and the mitogen-activated protein kinase signalling cascade. Although blockade of these pathways in animals has achieved a truly remarkable degree of neuroprotection of the neuron cell soma, it has not achieved protection of axons. Thus, there is a need to explore beyond the canonical pathways of PCD and investigate mechanisms of axon destruction. We also need to move beyond the narrow classic concept that the mechanisms of PCD are activated exclusively 'downstream', following cellular injury. Studies in the genetics of PD suggest that in some forms of the disease, activation may be an early 'upstream' event. Additionally, recent observations suggest that cell death in some contexts may not be initiated by injury, but instead by a failure of intrinsic cell survival signalling. These new points of view offer new opportunities for molecular targeting.

Indexed as

AnimalsApoptosisAxonsDopamineGlial Cell Line-Derived Neurotrophic FactorHumansIntracellular Signaling Peptides and ProteinsLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Nerve DegenerationNeuronsOncogene ProteinsParkinson DiseaseProtein Deglycase DJ-1Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktDopamineGlial Cell Line-Derived Neurotrophic FactorIntracellular Signaling Peptides and ProteinsLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanOncogene ProteinsPARK7 protein, humanProtein Deglycase DJ-1Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPTEN-Induced Putative Kinase

Identifiers

PMID20696316
PMCPMC3088517
OpenAlexW1510654197

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.