Elsevier

Schizophrenia Research

Volume 67, Issue 1, 1 March 2004, Pages 111-113
Schizophrenia Research

Letter to the Editors
Failure to find association between PRODH deletion and schizophrenia

https://doi.org/10.1016/S0920-9964(03)00160-9Get rights and content

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Cited by (23)

  • Association of COMT and PRODH gene variants with intelligence quotient (IQ) and executive functions in 22q11.2DS subjects

    2014, Journal of Psychiatric Research
    Citation Excerpt :

    A deficit in associative learning was detected in a mouse model of PRODH deficiency that mimics the status in 22q11.2DS (Paterlini et al., 2005). Several human studies failed to find an association between the various PRODH gene variants and schizophrenia (Glaser et al., 2006b; Abou Jamra et al., 2005; Ohtsuki et al., 2004; Williams et al., 2003a, 2003b; Fan et al., 2003). However, they did not assess the impact of the PRODH gene variants on EF and IQ.

  • Schizophrenia genetics: Progress, at last

    2012, Current Opinion in Genetics and Development
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    Estimates of psychosis in adult VCFS patients with 22q11 deletion range from 6 to 16% [35,36] a recent study estimates the rate of DSM IV SZ diagnosis in 78 adults with 22q deletion syndrome at 22.6% [37], a more than 20-fold increase in the rate of SZ in the general population. Proline dehydrogenase, a gene in the 22q11 deletion interval, was reported associated with SZ [38,39]; other reports suggest this gene is not associated with schizophrenia [40–42]. The COMT gene has also been extensively studied, but no consensus exists on identified susceptibility variants [43–46].

  • Functional consequences of PRODH missense mutations

    2005, American Journal of Human Genetics
    Citation Excerpt :

    It would be important to restudy these individuals, to determine if their phenotypes were typical of schizophrenia or if, in retrospect, there were any unusual features (age at onset, response to therapy, etc.). PRODH variants have also been implicated as susceptibility factors for schizophrenia and schizoaffective disorder in some (Gogos et al. 1999; Chakravarti 2002; Jacquet et al. 2002, 2004; Liu et al. 2002b; Hoogendoorn et al. 2004; Li et al. 2004) but not all studies (Williams et al. 2003a, 2003b; Ohtsuki et al. 2004). To account for increased susceptibility for a common phenotype, a locus must have a substantial reservoir of variation (Reich and Lander 2001; Pritchard and Cox 2002), and this is the case for PRODH (see table 1).

  • Contribution of non primate animal models in understanding the etiology of schizophrenia

    2011, Journal of Psychiatry and Neuroscience
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    Other studies have also implicated this gene in the development of schizophrenia in a Chinese family233 and in individuals affected with schizoaffective disorder.234 However, other studies have not found such an association.235–237 Despite some inconsistency in the results, taken together, the evidence seems to suggest that mutations in PRODH are implicated in the etiology of schizophrenia.

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This study was supported by the grant of Research on Brain Science and the grant for Nervous and Mental Disorders from the Ministry of Health, Labor and Welfare, and Grant-in-Aid for Scientific Research on Priority Areas “Medical Genome Science” from the Ministry of Education, Culture, Sports, Science and Technology of Japan.

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