Evidence map›Paper›PMID 24681994›Full record

ReviewMolecular medicine reports2014

Association of glycogen synthase kinase-3β with Parkinson's disease (review).

Da-Wei Li, Zhi-Qiang Liu, Wei Chen, Min Yao, Guang-Ren Li

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular medicine reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
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  4. Review
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  7. Review
  8. Review
  9. Positive Effects of Argon Inhalation After Traumatic Brain Injury in Rats.International journal of molecular sciences · 2024
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  14. Potential Neuroprotective Role of Neurotrophin in Traumatic Brain Injury.CNS & neurological disorders drug targets · 2024
    Review
  15. Article
  16. Marine-derived Compounds: A Powerful Platform for the Treatment of Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024
    Review
  17. Therapeutic potential for KCC2-targeted neurological diseases.The Japanese dental science review · 2023
    Review
  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

5 authors at 3 institutions in 1 country.

Da-Wei LiDepartment of Neurology, Affiliated Hospital of Beihua University, Jilin, Jilin 132000, P.R. China.
Zhi-Qiang LiuDepartment of Neurology, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Wei ChenDepartment of Neurology, The Third Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Min YaoDepartment of Neurology, The Third Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Guang-Ren LiDepartment of Neurology, The Third Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Jilin University · CNBeihua University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase-3 (GSK-3) is a pleiotropic serine/threonine protein kinase found in almost all eukaryotes. It is structurally highly conserved and has been identified as a multifaceted enzyme affecting a wide range of biological functions, including gene expression and cellular processes. There are two closely related isoforms of GSK-3; GSK-3α and GSK-3β. The latter appears to play crucial roles in regulating the pathogenesis of diverse diseases, including neurodegenerative disease. The present review focuses on the involvement of this protein in Parkinson's disease (PD), a common neurodegenerative disorder characterized by the gradually progressive and selective loss of dopaminergic neurons, and by intracellular inclusions known as Lewy bodies (LBs) expressed in surviving neurons of the substantia nigra (SN). GSK-3β is involved in multiple signaling pathways and has several phosphorylation targets. Numerous apoptotic conditions can be facilitated by the GSK-3β signaling pathways. Studies have shown that GSK-3β inhibition protects the dopaminergic neurons from various stress-induced injuries, indicating the involvement of GSK-3β in PD pathogenesis. However, the underlying mechanisms of the protective effect of GSK-3β inhibition on dopaminergic neurons in PD is not completely understood. Multiple pathological events have been recognized to be responsible for the loss of dopaminergic neurons in PD, including mitochondrial dysfunction, oxidative stress, protein aggregation and neuroinflammation. The present review stresses the regulatory roles of GSK-3β in these events and in dopaminergic neuron degeneration, in an attempt to gain an improved understanding of the underlying mechanisms and to provide a potential effective therapeutic target for PD.

Indexed as

alpha-SynucleinAnimalsApoptosisBrachyury ProteinElectron Transport Complex IFetal ProteinsGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInflammationMitochondriaParkinson DiseaseReactive Oxygen SpeciesSignal TransductionT-Box Domain Proteinsalpha-SynucleinBrachyury ProteinElectron Transport Complex IFetal ProteinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanReactive Oxygen SpeciesT-Box Domain Proteins

Identifiers

PMID24681994
PMCPMC4055480
OpenAlexW1969074927

What OpenQuestion holds

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Registered trials

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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.