Evidence map›Paper›PMID 23628988›Full record

ReviewMolecular psychiatry2013

What psychiatric genetics has taught us about the nature of psychiatric illness and what is left to learn.

Kenneth S Kendler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. The Emerging Role of the DDAH Proteins in Psychiatric Disorders.Biological psychiatry global open science · 2025
    Review
  7. Article
  8. Philosophy of psychiatry: theoretical advances and clinical implications.World psychiatry : official journal of the World Psychiatric Association (WPA) · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Axonal transport deficits in neuropsychiatric disorders.Molecular and cellular neurosciences · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Involvement of Scratch2 in GalR1-mediated depression-like behaviors in the rat ventral periaqueductal gray.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Article
  20. Review

3 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

1 author.

Kenneth S KendlerVirginia Institute of Psychiatric and Behavioral Genetics, and Departments of Psychiatry, and Human and Molecular Genetics, School of Medicine/Virginia Commonwealth University, Richmond, VA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psychiatric genetics has taught us a great deal about the nature of psychiatric disorders. Traditional family, twin and adoption studies have demonstrated the substantial role of genetic factors in their etiology, clarified the role of genetic factors in comorbidity, elucidated development pathways, and documented the importance of gene-environment correlation and interaction. We have also received some hard lessons when we were unable to detect replicable genes of large effect size and found that our much-valued candidate genes did not live up to their expected promise. With more mature molecular and statistical methods, we are entering now a different era. Statistical analyses of aggregate molecular signals are validating earlier heritability estimates. Replicated findings from genome-wide association studies are beginning to emerge, as are discoveries of large-effect size rare genomic variants. The number of such findings is likely to soon grow dramatically. The most pressing question facing the field is what biological picture these results will reveal. I articulate four possible scenarios that reflect (i) no, (ii) minimal, (iii) moderate and (iv) high biological coherence in the replicated molecular variant findings, which are soon likely to emerge. I discuss the factors that will likely influence these patterns, including the problems of etiological heterogeneity and multiple realizability. These findings could provide critical insights into the underlying biology of our psychiatric syndromes and potentially permit us to perceive, 'through a glass darkly,' the levels of the mind-brain system that are disordered.

Indexed as

Genetics, BehavioralAdoptionCase-Control StudiesCausalityGene-Environment InteractionGenetic Association StudiesGenetic HeterogeneityGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMental DisordersModels, GeneticModels, NeurologicalModels, PsychologicalPolymorphism, Single NucleotideQuantitative Trait, Heritable

Identifiers

PMID23628988

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.