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Article

Nogo A, B and C expression in schizophrenia, depression and bipolar frontal cortex, and correlation of Nogo expression with CAA/TATC polymorphism in 3'-UTR.

Brain research - 20 Nov 2006

Novak Gabriela, Tallerico Teresa

Abstract excerpt

Schizophrenia may result from altered gene expression leading to abnormal neurodevelopment. In a search for genes with altered expression in schizophrenia, our previous work on human frontal cerebral cortex found the mRNA of Nogo, a myelin-associated protein which inhibits the outgrowth of neurites and nerve terminals, to be overexpressed in schizophrenia. Because those earlier results did not examine tissues for...

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Identifiers

PMID: 17022955
DOI: 10.1016/j.brainres.2006.08.071

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Nogo A, B and C expression in schizophrenia, depression and bipolar frontal cortex, and correlation of Nogo expression with CAA/TATC polymorphism in 3'-UTR.PMID 17022955Read ↗

Schizophrenia and Nogo: elevated mRNA in cortex, and high prevalence of a homozygous CAA insert.Semantic proximity Read ↗

Nogo CAA 3'UTR Insertion polymorphism is not associated with Schizophrenia nor with bipolar disorder.Semantic proximity Read ↗

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Genetic variants of Nogo-66 receptor with possible association to schizophrenia block myelin inhibition of axon growth.Semantic proximity Read ↗

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