Susceptibility locus on chromosome 1q23-25 for a schizophrenia subtype resembling deficit schizophrenia identified by latent class analysis

Arch Gen Psychiatry. 2009 Oct;66(10):1058-67. doi: 10.1001/archgenpsychiatry.2009.136.

Abstract

Context: Identifying susceptibility genes for schizophrenia may be complicated by phenotypic heterogeneity, with some evidence suggesting that phenotypic heterogeneity reflects genetic heterogeneity.

Objective: To evaluate the heritability and conduct genetic linkage analyses of empirically derived, clinically homogeneous schizophrenia subtypes.

Design: Latent class and linkage analysis.

Setting: Taiwanese field research centers.

Participants: The latent class analysis included 1236 Han Chinese individuals with DSM-IV schizophrenia. These individuals were members of a large affected-sibling-pair sample of schizophrenia (606 ascertained families), original linkage analyses of which detected a maximum logarithm of odds (LOD) of 1.8 (z = 2.88) on chromosome 10q22.3.

Main outcome measures: Multipoint exponential LOD scores by latent class assignment and parametric heterogeneity LOD scores.

Results: Latent class analyses identified 4 classes, with 2 demonstrating familial aggregation. The first (LC2) described a group with severe negative symptoms, disorganization, and pronounced functional impairment, resembling "deficit schizophrenia." The second (LC3) described a group with minimal functional impairment, mild or absent negative symptoms, and low disorganization. Using the negative/deficit subtype, we detected genome-wide significant linkage to 1q23-25 (LOD = 3.78, empiric genome-wide P = .01). This region was not detected using the DSM-IV schizophrenia diagnosis, but has been strongly implicated in schizophrenia pathogenesis by previous linkage and association studies.Variants in the 1q region may specifically increase risk for a negative/deficit schizophrenia subtype. Alternatively, these results may reflect increased familiality/heritability of the negative class, the presence of multiple 1q schizophrenia risk genes, or a pleiotropic 1q risk locus or loci, with stronger genotype-phenotype correlation with negative/deficit symptoms. Using the second familial latent class, we identified nominally significant linkage to the original 10q peak region.

Conclusion: Genetic analyses of heritable, homogeneous phenotypes may improve the power of linkage and association studies of schizophrenia and thus have relevance to the design and analysis of genome-wide association studies.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Chromosome Mapping*
  • Chromosomes, Human, Pair 1 / genetics*
  • Diagnostic and Statistical Manual of Mental Disorders
  • Female
  • Genetic Heterogeneity
  • Genetic Linkage / genetics
  • Genetic Predisposition to Disease / genetics*
  • Genome, Human
  • Genome-Wide Association Study
  • Genotype
  • Humans
  • Male
  • Models, Statistical
  • Multivariate Analysis
  • Phenotype
  • Psychiatric Status Rating Scales / statistics & numerical data
  • Schizophrenia / classification
  • Schizophrenia / diagnosis*
  • Schizophrenia / genetics*
  • Taiwan