Convergent evidence for impaired AKT1-GSK3β signaling in schizophrenia View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2004-02

AUTHORS

Effat S Emamian, Diana Hall, Morris J Birnbaum, Maria Karayiorgou, Joseph A Gogos

ABSTRACT

AKT-GSK3beta signaling is a target of lithium and as such has been implicated in the pathogenesis of mood disorders. Here, we provide evidence that this signaling pathway also has a role in schizophrenia. Specifically, we present convergent evidence for a decrease in AKT1 protein levels and levels of phosphorylation of GSK3beta at Ser9 in the peripheral lymphocytes and brains of individuals with schizophrenia; a significant association between schizophrenia and an AKT1 haplotype associated with lower AKT1 protein levels; and a greater sensitivity to the sensorimotor gating-disruptive effect of amphetamine, conferred by AKT1 deficiency. Our findings support the proposal that alterations in AKT1-GSK3beta signaling contribute to schizophrenia pathogenesis and identify AKT1 as a potential schizophrenia susceptibility gene. Consistent with this proposal, we also show that haloperidol induces a stepwise increase in regulatory phosphorylation of AKT1 in the brains of treated mice that could compensate for an impaired function of this signaling pathway in schizophrenia. More... »

PAGES

131-137

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng1296

DOI

http://dx.doi.org/10.1038/ng1296

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043172518

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14745448


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