Evidence map›Paper›PMID 23705847›Full record

ArticleMolecular brain2013

Neurological characterization of mice deficient in GSK3α highlight pleiotropic physiological functions in cognition and pathological activity as Tau kinase.

Hervé Maurin, Benoit Lechat, Ilse Dewachter, Laurence Ris, Justin V Louis, Peter Borghgraef, Herman Devijver, Tomasz Jaworski, Fred Van Leuven

Abstract read
In one paragraph

Article in Molecular brain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

24 citing papers in PubMed.

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  15. Dopamine DJournal of biomedical science · 2020
    Article
  16. GSK-3Neural plasticity · 2019
    Review
  17. Article
  18. Article
  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

9 authors.

Hervé MaurinDepartment Human Genetics, Experimental Genetics Group - LEGTEGG, KULeuven, Leuven, Belgium.
Benoit Lechat
Ilse Dewachter
Laurence Ris
Justin V Louis
Peter Borghgraef
Herman Devijver
Tomasz Jaworski
Fred Van Leuven

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGSK3β is involved in a wide range of physiological functions, and is presumed to act in the pathogenesis of neurological diseases, from bipolar disorder to Alzheimer's disease (AD). In contrast, the GSK3α isozyme remained largely ignored with respect to both aspects.

resultsWe generated and characterized two mouse strains with neuron-specific or with total GSK3α deficiency. Behavioral and electrophysiological analysis demonstrated the physiological importance of neuronal GSK3α, with GSK3β not compensating for impaired cognition and reduced LTP. Interestingly, the passive inhibitory avoidance task proved to modulate the phosphorylation status of both GSK3 isozymes in wild-type mice, further implying both to function in cognition. Moreover, GSK3α contributed to the neuronal architecture of the hippocampal CA1 sub-region that is most vulnerable in AD. Consequently, practically all parameters and characteristics indicated that both GSK3 isoforms were regulated independently, but that they acted on the same physiological functions in learning and memory, in mobility and in behavior.

conclusionsGSK3α proved to be regulated independently from GSK3β, and to exert non-redundant physiological neurological functions in general behavior and in cognition. Moreover, GSK3α contributes to the pathological phosphorylation of protein Tau.

Indexed as

Genetic PleiotropyAnimalsBehavior, AnimalBody WeightBrainCA1 Region, HippocampalCognitionCrosses, GeneticFemaleGenotypeGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInfertility, MaleIntegrasesIsoenzymesCre recombinaseGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseIntegrasesIsoenzymesMutant Proteinstau Proteins

Identifiers

PMID23705847
PMCPMC3671145

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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.