Evidence map›Paper›PMID 19634037›Full record

ArticleCognitive neuropsychiatry2009

Genome-wide strategies for discovering genetic influences on cognition and cognitive disorders: methodological considerations.

Steven G Potkin, Jessica A Turner, Guia Guffanti, Anita Lakatos, Federica Torri, David B Keator, Fabio Macciardi

Open access · greenAbstract read
In one paragraph

Article in Cognitive neuropsychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Brain Imaging Genomics: Integrated Analysis and Machine Learning.Proceedings of the IEEE. Institute of Electrical and Electronics Engineers · 2020
    Article
  10. Genome-wide association study identifiesAnnals of translational medicine · 2018
    Article
  11. Article
  12. Review
  13. Longitudinal Genotype-Phenotype Association Study through Temporal Structure Auto-Learning Predictive Model.Journal of computational biology : a journal of computational molecular cell biology · 2018
    Article
  14. Article
  15. Genotype-phenotype association study via new multi-task learning model.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2018
    Article
  16. Article
  17. Identifying Associations Between Brain Imaging Phenotypes and Genetic Factors via A Novel Structured SCCA Approach.Information processing in medical imaging : proceedings of the ... conference · 2017
    Article
  18. Longitudinal Genotype-Phenotype Association Study via Temporal Structure Auto-Learning Predictive Model.Research in computational molecular biology : ... Annual International Conference, RECOMB ... : proceedings. RECOMB (Conference : 2005- ) · 2017
    Article
  19. Article
  20. Review

2 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

7 authors at 3 institutions in 2 countries.

Steven G PotkinDepartment of Psychiatry and Human Behavior, University California of Irvine, Irvine, CA, USA. sgpotkin@uci.edu
Jessica A Turner
Guia Guffanti
Anita Lakatos
Federica Torri
David B Keator
Fabio Macciardi
University of California, Irvine · USFondazione Filarete · ITUniversity of Milan · IT

Funding

FUNCTION BIRNU24RR021992 · NCRR · UNIVERSITY OF CALIFORNIA-IRVINE · PI POTKIN, STEVEN G · 2006 to 2010
$25.0M
NCRR NIH HHS U24 RR021992
6 · The paper itself

Abstract

introductionGenes play a well-documented role in determining normal cognitive function. This paper focuses on reviewing strategies for the identification of common genetic variation in genes that modulate normal and abnormal cognition with a genome-wide association scan (GWAS). GWASs make it possible to survey the entire genome to discover important but unanticipated genetic influences.

methodsThe use of a quantitative phenotype in combination with a GWAS provides many advantages over a case-control design, both in power and in physiological understanding of the underlying cognitive processes. We review the major features of this approach, and show how, using a General Linear Model method, the contribution of each Single Nucleotide Polymorphism (SNP) to the phenotype is determined, and adjustments then made for multiple tests. An example of the strategy is presented, in which fMRI measures of cortical inefficiency while performing a working memory task are used as the quantitative phenotype. We estimate power under different effect sizes (10-30%) and variations in allelic frequency for a Quantitative Trait (QT) (10-20%), and compare them to a case-control design with an Odds Ratio (OR) of 1.5, showing how a QT approach is superior to a traditional case-control. In the presented example, this method identifies putative susceptibility genes for schizophrenia which affect prefrontal efficiency and have functions related to cell migration, forebrain development and stress response.

conclusionThe use of QT as phenotypes provide increased statistical power over categorical association approaches and when combined with a GWAS creates a strategy for identification of unanticipated genes that modulate cognitive processes and cognitive disorders.

Indexed as

AlgorithmsCognitionCognition DisordersGene FrequencyGenome-Wide Association StudyGenomicsHumansModels, GeneticModels, NeurologicalModels, StatisticalPhenotypePolymorphism, Single Nucleotide

Identifiers

PMID19634037
PMCPMC3037334
OpenAlexW1983261448

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.