Evidence map›Paper›PMID 15618952›Full record

ReviewMolecular psychiatry2005

Genetic heterogeneity, modifier genes, and quantitative phenotypes in psychiatric illness: searching for a framework.

A H Fanous, K S Kendler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  4. Pooled it
  5. Article
  6. Article
  7. Locus-Specific Genetic Associations at theAdvanced genetics (Hoboken, N.J.) · 2026
    Article
  8. Protein interacting with C-kinase 1 (PICK1) regulates synaptic function and reversal learning in a mouse model for schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  9. Article
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  13. Review
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  15. Article
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  17. Article
  18. Evidence of an interaction betweenEuropean psychiatry : the journal of the Association of European Psychiatrists · 2021
    Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

A H FanousWashington VA Medical Center, Georgetown University Medical Center Schizophrenia Research Program, Washington DC 20008, USA. ayman.fanous@med.va.gov
K S Kendler

Funding

Research Training: Psychiatric &Statistical GeneticsT32MH020030 · NIMH · VIRGINIA COMMONWEALTH UNIVERSITY · PI HERMINE H MAES, MICHAEL CHURTON NEALE · 1999 to 2026
$6.7M
THE GENETIC EPIDEMIOLOGY OF SCHIZOPHRENIA IN IRELANDR01MH041953 · NIMH · VIRGINIA COMMONWEALTH UNIVERSITY · PI KENDLER, KENNETH SEEDMAN · 1987 to 2008
$5.2M
MOLECULAR GENETICS OF SCHIZOPHENIAR01MH045390 · NIMH · VIRGINIA COMMONWEALTH UNIVERSITY · PI STRAUB, RICHARD ERIC · 1989 to 1999
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GENOMEWIDE SEARCH FOR SCHIZOPHRENIA SUSCEPTIBILITY LOCIR01MH052537 · NIMH · VIRGINIA COMMONWEALTH UNIVERSITY · PI MACLEAN, CHARLES J · 1995 to 1998
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NIMH NIH HHS IT-32 MH-20030NIMH NIH HHS MH-41953NIMH NIH HHS MH-45390NIMH NIH HHS MH-52537
6 · The paper itself

Abstract

Schizophrenia has long been thought to be clinically heterogeneous. A range of studies suggests that this is due to genetic heterogeneity. Some clinical features, such as negative symptoms, are associated with a greater risk of illness in relatives. Affected sibling pairs are correlated for clinical and course features as well as subforms of illness, and twin studies suggest that this is due to genetic factors. This is further supported by findings that subjects from families linked to some chromosomal regions may differ clinically from those from unlinked families. Moreover, some genes may affect clinical features without altering susceptibility (ie are modifier genes). High-risk genotypes may have quantitative, rather than categorical effects, and may influence milder or subclinical phenotypes. Another recent finding is that nonpsychotic relatives may have personality features that resemble those of their affected relatives. These findings taken together suggest that there may be several classes of gene action in schizophrenia: some genes may influence susceptibility only, others may influence clinical features only, and still others may have a mixed effect. Furthermore, subsets of these classes may affect personality and other traits in nonpsychotic relatives. Understanding these classes of gene action may help guide the design of linkage and association studies that have increased power. We describe five classes of genes and their predictions of the outcomes of family, twin, and several types of linkage studies. We go on to explore how these predictions can in turn be used to aid in the design of linkage studies.

Indexed as

Models, GeneticGenetic LinkageGenetic Predisposition to DiseaseGenetic VariationHumansLod ScoreMental DisordersPedigreeSchizophrenia

Identifiers

PMID15618952

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.