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Budel S, Padukkavidana T, Liu BP, Feng Z, Hu F, Johnson S, Lauren J, Park JH, McGee AW, Liao J, Stillman A, Kim JE, Yang BZ, Sodi S, Gelernter J, Zhao H, Hisama F, Arnsten AF, Strittmatter SM. Genetic variants of Nogo-66 receptor with possible association to schizophrenia block myelin inhibition of axon growth. J Neurosci . 2008 Dec 3 ; 28(49):13161-72. PubMed Abstract

Comments on Paper and Primary News
Primary News: Do Faulty Nogo Receptors Allow Axons to Run Amuck in Schizophrenia?

Comment by:  Takeshi SakuraiJoseph D. BuxbaumPatrick R. Hof
Submitted 9 January 2009 Posted 9 January 2009

Several lines of evidence indicate that oligodendrocytes and myelin are disturbed in schizophrenia (Davis et al., 2003; Segal et al., 2007). However, the relationship of these alterations to the pathogenesis of schizophrenia is still unclear. A recent paper by Budel et al. proposes one possible link between oligodendrocyte and myelin pathology and schizophrenia pathogenesis. The gene for Nogo-66 receptor 1 (RTN4R) is located within the 22q11.2 locus where a hemizygous microdeletion (1.5 Mb) occurs at a frequency of one in 5,000. Twenty to 30 percent of individuals with the deletion develop schizophrenia. Several candidate genes for the schizophrenia phenotype within this locus have been characterized for genetic association, and common variants of the Nogo-66 receptor 1 gene have shown association in one study (Liu et al., 2002), but replication studies have not confirmed the findings using different cohorts (  Read more

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Primary News: Do Faulty Nogo Receptors Allow Axons to Run Amuck in Schizophrenia?

Comment by:  Ruby Hsu
Submitted 9 February 2009 Posted 10 February 2009

Individuals with hemizygous microdeletions at the 22q11.2 locus display a range of cognitive and behavioral deficits, and compared to the general population these individuals have a greatly increased risk of developing schizophrenia (Karayiorgou et al., 1995). A number of candidate schizophrenia susceptibility genes have been identified within the 22q11.2 region (Mukai et al., 2004; Paterlini et al., 2005; Paylor et al., 2006; Stark et al., 2008). In our paper (Hsu et al., 2007), we evaluated RTN4R (NgR1), one of the genes in the 22q11.2 region, as a schizophrenia susceptibility gene using a variety of approaches including human association analyses as well as mouse behavioral and anatomical assays. We evaluated common RTN4R variants in a large Afrikaner family sample and found RTN4R polymorphisms which...  Read more

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Primary News: Do Faulty Nogo Receptors Allow Axons to Run Amuck in Schizophrenia?

Comment by:  Georgia Karoutzou
Submitted 26 February 2009 Posted 26 February 2009

This is a thorough and generally well-written manuscript that provides further evidence to the hypothesis that schizophrenia may be viewed as a disconnectivity syndrome (Frith, 1996; Davis et al., 2003) due to disturbances in myelination.

Even though the authors examined a large sample consisting of 3 different populations (Caucasians, African-Americans and Chinese Han trio sample), they do not provide details regarding the age-ratio of these populations, nor do they report the treatment of these patients. Hence, there is a growing body of evidence of age-related changes in the human brain (Allen et al., 2005).We consider that the authors of this study fail to investigate of how the effects of age are expressed. It can not be ruled out whether there is any effect of the medication in the observed results. Even though medication is not implicated in the observed alterations in gene expression in schizophrenia in several studies (  Read more

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