Hostname: page-component-cd9895bd7-dk4vv Total loading time: 0 Render date: 2024-12-25T18:58:35.590Z Has data issue: false hasContentIssue false
  • English
  • Français

Early development and unstable genes in schizophrenia: preliminary results

Published online by Cambridge University Press:  16 April 2020

Agnes Ayton ,
Alex G. Morris ,
Philip J. Tyson ,
David Hunt ,
Ann M. Mortimer  and
David Cottrell
Agnes Ayton*
Affiliation:
Department of Psychiatry, University of Hull, East Riding Campus, Coniston House, Willerby, East YorkshireHU10 6NS, UK
Alex G. Morris
Affiliation:
Institute of Ophthalmology, UCL 43 Bath Street, London, EC1V 9EL, UK
Philip J. Tyson
Affiliation:
Department of Psychiatry, University of Hull, East Riding Campus, Coniston House, Willerby, East YorkshireHU10 6NS, UK
David Hunt
Affiliation:
Institute of Ophthalmology, UCL 43 Bath Street, London, EC1V 9EL, UK
Ann M. Mortimer
Affiliation:
Department of Psychiatry, University of Hull, East Riding Campus, Coniston House, Willerby, East YorkshireHU10 6NS, UK
David Cottrell
Affiliation:
Academic Unit of Child and Adolescent Mental Health, 12Clarendon Rd, LeedsLS2 9NN, UK
*
*E-mail address:A.K.Ayton@hull.ac.uk (A. Ayton).
Get access

Summary

Background.

Trinucleotide repeats have been associated with schizophrenia, but the evidence, based on cross-sectional clinical information, is equivocal.

Aims.

To examine the relationship between genomic CAG/CTG repeat size and premorbid development in schizophrenia.

Method.

Early development and premorbid functioning of 22 patients with DSM-IV diagnosis of schizophrenia were assessed by parental interviews. Repeat expansion detection (RED) technique was used to measure genomic CAG/CTG repeat size, and PCR for CAG repeat size at the ERDA-1 and CTG 18.1 loci.

Results.

There was an inverse association between CAG/CTG size and perinatal complications. Patients with speech and motor developmental delay had larger repeats. The results were not due to expansion in the ERDA-1 and CTG 18.1 genes.

Conclusions.

CAG/CTG repeat expansion is associated with speech and motor developmental delay in schizophrenia. We propose that the developmental model may be useful for research into the genetics of schizophrenia.

Keywords

SchizophreniaEarly development–geneticsTrinucleotide repeats
Type
Original article
Information
European Psychiatry , Volume 17 , Issue 6 , October 2002 , pp. 332 - 338
Copyright
Copyright © Éditions scientifiques et médicales Elsevier SAS 2002

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

American Psychiatric Association. Global assessment of functioning scale. In: American Psychiatric Association, editor. DSM-III-R: diagnostic and statistical manual of mental disorders. Washington: APA; 1984.Google Scholar
Barkley, RA. Attention-deficit hyperactivity disorder: a handbook for diagnosis and treatment. The Guilford Press; 1990. p. 261–5.Google Scholar
Bassett, ASChow, EW. 22q11 deletion syndrome: a genetic subtype of schizophrenia. Biol Psychiatry 1999;46(7):882–91.Google ScholarPubMed
Bowen, TGuy, CACardno, AGVincent, JBKennedy, JLJones, LAet al. Repeat sizes at CAG/CTG loci CTG18.1, ERDA1 and TGCa13-7a in schizophrenia. Psych Genet 2000;10(1):33–7.CrossRefGoogle Scholar
Burgess, CELindblad, KSidransky, EYuan, QPLong, RTBreschel, Tet al. Large CAG/CTG repeats are associated with childhood-onset schizophrenia. Mol Psychiatry 1998;3(4):321–7.CrossRefGoogle ScholarPubMed
Cannon-Spoor, HEPotkin, SGWyatt, RJ. Measurement of premorbid adjustment in chronic schizophrenia. Schizophr Bull 1982;8(3):470–84.CrossRefGoogle ScholarPubMed
Cardno, AGMurphy, KCJones, LAGuy, CAAsherson, PDe Azevedo, MHet al. Expanded CAG/CTG repeats in schizophrenia. A study of clinical correlates. Br J Psychiatr 1996;169(6):766–71.CrossRefGoogle ScholarPubMed
Heun, RMaier, W. The role of obstetric complications in schizophrenia. J Nerv Ment Dis 1993; 181(4):220–6.CrossRefGoogle Scholar
Jones, PRodgers, BMurray, RMarmot, M. Child development risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet 1994;8934:1398–402.CrossRefGoogle Scholar
Jones, PBDone, DJ. From birth to onset: a developmental perspective of schizophrenia in two national birth cohorts. In: Keshavan, MSMurray, RM editors. Neurodevelopment and Adult Psychopathology. Cambridge: Cambridge University Press; 1997. p. 119–36.Google Scholar
Jones, PBRantakallio, PHartikainen, ALIsohanni, MSipila, P. Schizophrenia as a long-term outcome of pregnancy, delivery, and perinatal complications: a 28-year follow-up of thenorth Finland general population birth cohort. Am J Psychiatry 1998;155(3):355–64.CrossRefGoogle Scholar
Joober, RBenkelfat, CJannatipour, MTurecki, GLal, SMandel, JLet al. Polyglutamine-containing proteins in schizophrenia 〚see comments〛. Mol Psychiatry 1999;4(1):53–7.CrossRefGoogle Scholar
Margolis, RLMcInnis, MGRosenblatt, ARoss, CA. Trinucleotide repeat expansion and neuropsychiatric disease. 〚Review〛 〚211 refs〛. Arch Gen Psychiatry 1999;56(11):1019–31.CrossRefGoogle Scholar
McInnis, MGSwift-Scanlanl, TMahoney, ATVincent, JVerheyen, GLan, THet al. Allelic distribution of CTG18.1 in Caucasian populations: association studies in bipolar disorder, schizophrenia, and ataxia. Mol Psychiatry 2000;5(4):439–42.CrossRefGoogle ScholarPubMed
McNeil, TFCantor-Graae, ETorrey, EFSjostrom, KBowler, ATaylor, Eet al. Obstetric complications in histories of monozygotic twins discordant and concordant for schizophrenia. Acta Psychiatr Scand 1994;89(3):196–204.CrossRefGoogle Scholar
Moriniere, SSaada, CHolbert, SSidransky, EGalat, AGinns, Eet al. Detection of polyglutamine expansion in a new acidic protein: a candidate for childhood onset schizophrenia? 〚see comments〛. Mol Psychiatry 1999;4(1):58–63.Google Scholar
Morris, AGGaitonde, EMcKenna, PJMollon, JDHunt, DM. CAG repeat expansions and schizophrenia: association with disease in females and with early age-at-onset. Hum Mol Genet 1995;4(10):1957–61.CrossRefGoogle ScholarPubMed
Mortimer, AMMcKenna, PJLund, CEMannuzza, S. Rating of negative symptoms using the high Royds evaluation of negativity (HEN) scale. Br J Psychiatry 1989;(7) 〚Suppl〛:89–92.CrossRefGoogle ScholarPubMed
Murray, RMO’Callaghan, ECastle, DJLewis, SW. A neurodevelopmental approach to the classification of schizophrenia. 〚Review〛 〚90 refs〛. Schizophr Bull 1992;18(2):319–32.CrossRefGoogle Scholar
O'Donovan, MCGuy, CCraddock, NBowen, TMcKeon, PMacedo, Aet al. Confirmation of association between expanded CAG/CTG repeats and both schizophrenia and bipolar disorder. Psychol Med 1996;26(6):1145–53.Google ScholarPubMed
O’Donovan, MCOwen, MJ. Candidate-gene association studies of schizophrenia. 〚Review〛 〚37 refs〛. Am J Hum Genet 1999;65(3):587–92.CrossRefGoogle Scholar
Petronis, ABassett, ASHoner, WGVincent, JBTatuch, YSasaki, Tet al. Search for unstable DNA in schizophrenia families with evidence for genetic anticipation. Am J Hum Genet 1996;59(4):905–11.Google ScholarPubMed
Roy, MLanctot, GMerette, CCliche, DFournier, JPBoutin, Pet al. Clinical and methodological factors related to reliability of the best-estimate diagnostic procedure. Am J Psychiatry 1997;154(12):1726–33.CrossRefGoogle ScholarPubMed
Schalling, MHudson, TJBuetow, KHHousman, DE. Direct detection of novel expanded trinucleotide repeats in the human genome. Nature Genet 1993;4(2):135–9.CrossRefGoogle ScholarPubMed
Sidransky, EBurgess, CIkeuchi, TLindblad, KLong, RTPhilibert, RAet al. A triplet repeat on 17q accounts for most expansions detected by the repeat-expansion-detection technique. Am J Hum Genet 1998;62(6):1548–51.CrossRefGoogle ScholarPubMed
Sirugo, GDeinard, ASKidd, JRKidd, KK. Survey of maximum CTG/CAG repeat lengths in humans and non-human primates: total genome scan in populations using the repeat expansion detection (RED) method. Hum Mol Genet 1997;6(3):403–8.CrossRefGoogle ScholarPubMed
Verheyen, GRDel Favero, JMendlewicz, JLindblad, KVan Zand, KAalbregtse, Met al. Molecular interpretation of expanded RED products in bipolar disorder by CAG/CTG repeats located at chromosomes 17q and 18q. Neurobiol Disease 1999;6(5):424–32.Google ScholarPubMed
Submit a response

Comments

No Comments have been published for this article.