Evidence map›Paper›PMID 17785269›Full record

ArticleProceedings. Biological sciences2007

Adaptive evolution of genes underlying schizophrenia.

Bernard Crespi, Kyle Summers, Steve Dorus

Open access · greenAbstract read
In one paragraph

Article in Proceedings. Biological sciences, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 2% of its field
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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 185 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. The evolutionary origin of psychosis.Frontiers in psychiatry · 2023
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Antagonistic Pleiotropy in Human Disease.Journal of molecular evolution · 2020
    Review
  18. Review
  19. How evolutionary psychiatry can advance psychopharmacology
.Dialogues in clinical neuroscience · 2019
    Article
  20. Positive and balancing selection onEvolution letters · 2018
    Article
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

3 authors at 3 institutions in 3 countries.

Bernard CrespiDepartment of Biosciences, Simon Fraser University, Burnaby, British Columbia, Canada V5A 1S6. crespi@sfu.ca
Kyle Summers
Steve Dorus
East Carolina University · USSimon Fraser University · CAUniversity of Bath · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia poses an evolutionary-genetic paradox because it exhibits strongly negative fitness effects and high heritability, yet it persists at a prevalence of approximately 1% across all human cultures. Recent theory has proposed a resolution: that genetic liability to schizophrenia has evolved as a secondary consequence of selection for human cognitive traits. This hypothesis predicts that genes increasing the risk of this disorder have been subject to positive selection in the evolutionary history of humans and other primates. We evaluated this prediction using tests for recent selective sweeps in human populations and maximum-likelihood tests for selection during primate evolution. Significant evidence for positive selection was evident using one or both methods for 28 of 76 genes demonstrated to mediate liability to schizophrenia, including DISC1, DTNBP1 and NRG1, which exhibit especially strong and well-replicated functional and genetic links to this disorder. Strong evidence of non-neutral, accelerated evolution was found for DISC1, particularly for exon 2, the only coding region within the schizophrenia-associated haplotype. Additionally, genes associated with schizophrenia exhibited a statistically significant enrichment in their signals of positive selection in HapMap and PAML analyses of evolution along the human lineage, when compared with a control set of genes involved in neuronal activities. The selective forces underlying adaptive evolution of these genes remain largely unknown, but these findings provide convergent evidence consistent with the hypothesis that schizophrenia represents, in part, a maladaptive by-product of adaptive changes during human evolution.

Indexed as

Evolution, MolecularAnimalsGenetic Predisposition to DiseaseHumansPrimatesSchizophreniaSelection, GeneticSoftware

Identifiers

PMID17785269
PMCPMC2288689
OpenAlexW2158225568

What OpenQuestion holds

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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.