Major Psychosis and Chromosome 22: Genetics Meets Epigenetics

Petronis, Artūras; Popendikyte, Violeta; Kan, Peixiang; Sasaki, Tsukasa

doi:10.1017/s1092852900017570

Cited by 4 publications

(3 citation statements)

References 66 publications

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“…Genome scans for bipolar disorder have inferred linkages with maternal parent‐of‐origin effects for 1q41 and 13q12 (McInnis et al , 2003 b ), 2p24‐p21 and 2q31‐q32 (Cichon et al , 2001), and 22q13.1 (Petronis et al , 2002). By contrast, paternal parent‐of‐origin effects have been found for 16q21‐q23 (Cichon et al , 2001), 18p11 (Kato, 2001; see also Corradi et al , 2005), and 18q21‐q22 (McMahon et al , 2001; McInnis et al , 2003 b ; Schulze et al , 2003).…”

Section: Polygenic Effects: Genome Scan and Genetic Association Datamentioning

confidence: 99%

Genomic imprinting in the development and evolution of psychotic spectrum conditions

Crespi

2008

Biological Reviews

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I review and evaluate genetic and genomic evidence salient to the hypothesis that the development and evolution of psychotic spectrum conditions have been mediated in part by alterations of imprinted genes expressed in the brain. Evidence from the genetics and genomics of schizophrenia, bipolar disorder, major depression, Prader-Willi syndrome, Klinefelter syndrome, and other neurogenetic conditions support the hypothesis that the etiologies of psychotic spectrum conditions commonly involve genetic and epigenetic imbalances in the effects of imprinted genes, with a bias towards increased relative effects from imprinted genes with maternal expression or other genes favouring maternal interests. By contrast, autistic spectrum conditions, including Kanner autism, Asperger syndrome, Rett syndrome, Turner syndrome, Angelman syndrome, and Beckwith-Wiedemann syndrome, commonly engender increased relative effects from paternally expressed imprinted genes, or reduced effects from genes favouring maternal interests. Imprinted-gene effects on the etiologies of autistic and psychotic spectrum conditions parallel the diametric effects of imprinted genes in placental and foetal development, in that psychotic spectrum conditions tend to be associated with undergrowth and relatively-slow brain development, whereas some autistic spectrum conditions involve brain and body overgrowth, especially in foetal development and early childhood. An important role for imprinted genes in the etiologies of psychotic and autistic spectrum conditions is consistent with neurodevelopmental models of these disorders, and with predictions from the conflict theory of genomic imprinting.

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Section: Polygenic Effects: Genome Scan and Genetic Association Datamentioning

confidence: 99%

Genomic imprinting in the development and evolution of psychotic spectrum conditions

Crespi

2008

Biological Reviews

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“…A suggestion that schizophrenia might involve abnormalities of epigenetic control of gene expression (Petronis et al , 1999) has been increasingly favored in recent years (Petronis, 2000; Kan et al , 2004; Petronis et al , 2002; Petronis, 2004; Abdolmaleky et al , 2004; Grayson et al , 2005; Sharma, 2005; Wong et al , 2005). Major support for this hypothesis comes from the intriguing observation that approximately half of monozygotic twins are discordant for schizophrenia, although the risk of schizophrenia in the offspring of such twins is similar (Fischer, 1971).…”

Section: Discussionmentioning

confidence: 99%

Schizophrenia and birthplace of paternal and maternal grandfather in the Jerusalem perinatal cohort prospective study

Harlap

Perrin

Deutsch

et al. 2009

Schizophrenia Research

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Some forms of epigenetic abnormalities transmitted to offspring are manifest in differences in disease incidence that depend on parent-of-origin. To explore whether such phenomena might operate in schizophrenia spectrum disorders, we estimated the relative incidence of these conditions in relation to parent-of-origin by considering the two grandfathers' countries of birth. In a prospective cohort of 88,829 offspring, born in Jerusalem in 1964–76 we identified 637 cases through Israel's psychiatric registry. Relative risks (RR) were estimated for paternal and maternal grandfathers' countries of birth using proportional hazards methods, controlling for parents' ages, low social class and duration of marriage. After adjusting for multiple observations, we found no significant differences between descendants of maternal or paternal grandfathers born in Iraq, Iran, Turkey, Syria, Yemen, Morocco, Algeria, Tunisia, Libya/Egypt, Poland, USSR, Czechoslovakia, Germany or the USA. Those with paternal grandfathers from Romania (RR=1.9, 95% CI=1.3–2.8) or Hungary (1.6, 1.0–2.6) showed an increased incidence; however, those with maternal grandfathers from these countries experienced reduced incidence (RR=0.5, 0.3–0.8 and 0.4, 0.2–0.8). In post-hoc analyses we found that results were similar whether the comparison groups were restricted to descendants of other Europeans or included those from Western Asia and North Africa; and effects of paternal grandfathers from Romania/Hungary were more pronounced in females, while effects of maternal grandfathers from these countries were similar in males and females. These post-hoc “hypothesis-generating” findings lead one to question whether some families with ancestors in Romania or Hungary might carry a variant or mutation at a parentally imprinted locus that is altering susceptibility to schizophrenia. Such a locus, if it exists, might involve the X chromosome.

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“…Parent of origin-dependent clinical differences were also detected in schizophrenia (Crow et al 1989;Ohara et al 1997). Genetic linkage studies, although rarely performed in sex-specific fashion, also reveal parental origin effects in major psychosis (McMahon et al 1997;Petronis et al 2002;Schulze et al 2003). One of the most common mechanisms of parent-of-origin effects is genomic imprinting (Hall 1990).…”

Section: Parent-of-origin Effectsmentioning

confidence: 99%

Epigenetics of Complex Diseases: From General Theory to Laboratory Experiments

Schumacher

Petronis

Current Topics in Microbiology and Immunology

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Major Psychosis and Chromosome 22: Genetics Meets Epigenetics

Cited by 4 publications

References 66 publications

Genomic imprinting in the development and evolution of psychotic spectrum conditions

Genomic imprinting in the development and evolution of psychotic spectrum conditions

Schizophrenia and birthplace of paternal and maternal grandfather in the Jerusalem perinatal cohort prospective study

Epigenetics of Complex Diseases: From General Theory to Laboratory Experiments

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