title: Association of variants in DISC1 with psychosis-related traits in a large population cohort.
abstract: BACKGROUND
  There is an abundance of data from human genetic studies and animal models that implies a role for the disrupted in schizophrenia 1 gene (DISC1) in the etiology of schizophrenia and other major mental illnesses.
  
  
  OBJECTIVE
  To study the effect of previously identified risk alleles of DISC1 on quantitative intermediate phenotypes for psychosis in an unselected population.
  
  
  METHODS
  We examined 41 single-nucleotide polymorphisms within DISC1 and performed tests of association with 4 quantitative phenotypes.
  
  
  METHODS
  Academic research.
  
  
  METHODS
  Individuals from an unselected birth cohort in Finland. Originally, everyone born in the catchment area in 1966 (N = 12 058) was included in the study. Of these, 4651 (38.6%) attended the 31-year follow-up and could be included in the study.
  
  
  METHODS
  Scores on 4 psychometric instruments selected to function as proxies for positive and negative aspects of psychotic disorders, including the Perceptual Aberration Scale, Revised Social Anhedonia Scale, Revised Physical Anhedonia Scale, and Schizoidia Scale by Golden and Meehl.
  
  
  RESULTS
  Carriers of the minor allele of marker rs821577 had significantly higher scores on social anhedonia (P < .001). The minor allele of marker rs821633 was strongly associated with lower scores on social anhedonia when analyzed dependent on the absence of the minor alleles of markers rs1538979 and rs821577 (P < .001).
  
  
  CONCLUSIONS
  Variants in DISC1 affect the level of social anhedonia, a cardinal symptom of schizophrenia in the general population. DISC1 might be more central to human psychological functioning than previously thought, as it seems to affect the degree to which people enjoy social interactions.
authors.affiliation: Department of Molecular Medicine, National Public Health Institute, Helsinki, Finland. Jesper.Ekelund@ktl.fi
authors.forename: Liisa
authors.initials: L
authors.lastname: Tomppo
authors.forename: William
authors.initials: W
authors.lastname: Hennah
authors.forename: Jouko
authors.initials: J
authors.lastname: Miettunen
authors.forename: Marjo-Riitta
authors.initials: MR
authors.lastname: Järvelin
authors.forename: Juha
authors.initials: J
authors.lastname: Veijola
authors.forename: Samuli
authors.initials: S
authors.lastname: Ripatti
authors.forename: Päivi
authors.initials: P
authors.lastname: Lahermo
authors.forename: Dirk
authors.initials: D
authors.lastname: Lichtermann
authors.forename: Leena
authors.initials: L
authors.lastname: Peltonen
authors.forename: Jesper
authors.initials: J
authors.lastname: Ekelund
mesh_terms: D000328:Adult; D000342:Affective Symptoms / Q000235:genetics; D000483:Alleles; D015331:Cohort Studies; D005260:Female; D005387:Finland; D005500:Follow-Up Studies; D006580:Genetic Carrier Screening; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D011569:Psychiatric Status Rating Scales; D011618:Psychotic Disorders / Q000235:genetics* / Q000523:psychology; D012559:Schizophrenia / Q000235:genetics*; D012565:Schizophrenic Psychology; D012919:Social Behavior
chemical_list: C412476:DISC1 protein, human; D009419:Nerve Tissue Proteins