Evidence map›Paper›PMID 23812869›Full record

ArticleCerebellum (London, England)2013

Lithium chloride alleviates neurodegeneration partly by inhibiting activity of GSK3β in a SCA3 Drosophila model.

Dan-Dan Jia, Li Zhang, Zhao Chen, Chun-Rong Wang, Feng-Zhen Huang, Ran-Hui Duan, Kun Xia, Bei-Sha Tang, Hong Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Cerebellum (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Effects of lithium on aggression in Drosophila.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  5. International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Decreased NaScientific reports · 2020
    Article
  10. Genetics, Mechanisms, and Therapeutic Progress in Polyglutamine Spinocerebellar Ataxias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Therapies for ataxias.Current treatment options in neurology · 2014
    Article
  20. 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

9 authors at 2 institutions in 1 country.

Dan-Dan JiaDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, China.
Li Zhang
Zhao Chen
Chun-Rong Wang
Feng-Zhen Huang
Ran-Hui Duan
Kun Xia
Bei-Sha Tang
Hong Jiang
Xiangya Hospital Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinocerebellar ataxia type 3 (SCA3) is an autosomal dominant neurodegenerative disorder caused by the expansion of a CAG trinucelotide repeat that encodes an abnormal polyglutamine (PolyQ) tract in the disease protein, ataxin-3. The formation of neuronal intranuclear inclusions in the specific brain regions is one of the pathological hallmarks of SCA3. Acceleration of the degradation of the mutant protein aggregates is proven to produce beneficial effects in SCA3 and other PolyQ diseases. Lithium is known to be neuroprotective in various models of neurodegenerative disease and can reduce the mutant protein aggregates by inducing autophagy. In this study, we explored the therapeutic potential of lithium in a SCA3 Drosophila model. We showed that chronic treatment with lithium chloride at specific doses notably prevented eye depigmentation, alleviated locomotor disability, and extended the median life spans of SCA3 transgenic Drosophila. By means of genetic approaches, we showed that co-expressing the mutant S9E, which mimicked the phosphorylated S9 state of Shaggy as done by lithium, also partly decreased toxicity of gmr-SCA3tr-Q78. Taken together, our findings suggest that lithium is a promising therapeutic agent for the treatment of SCA3 and other PolyQ diseases.

Indexed as

Age FactorsAnimalsAnimals, Genetically ModifiedAtaxin-3Disease Models, AnimalDose-Response Relationship, DrugDrosophilaEnzyme ActivationEyeGene Expression RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansLithium ChlorideMicroscopy, Electron, ScanningMotor ActivityAtaxin-3ATXN3 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanLithium ChlorideNerve Tissue ProteinsNeuroprotective AgentsNuclear ProteinsPeptidespolyglutamineRepressor Proteins

Identifiers

PMID23812869
OpenAlexW2164650240

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.