Evidence map›Paper›PMID 17627031›Full record

ArticleNeuromolecular medicine2007

A linkage and family-based association analysis of a potential neurocognitive endophenotype of bipolar disorder.

Jonathan Savitz, Lize van der Merwe, Mark Solms, Rajkumar Ramesar

Abstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. 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

4 authors at 2 institutions in 1 country.

Jonathan SavitzDivision of Human Genetics, Institute for Infectious Disease and Molecular Medicine, University of Cape Town, South Africa. savitz@mail.nih.gov
Lize van der Merwe
Mark Solms
Rajkumar Ramesar
University of Cape Town · ZASouth African Medical Research Council · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The identification of the genetic variants underpinning bipolar disorder (BPD) has been impeded by a complex pattern of inheritance characterized by genetic and phenotypic heterogeneity, genetic epistasis, and gene-environment interactions. In this paper two strategies were used to ameliorate these confounding factors. A unique South African sample including 190 individuals of the relatively, reproductively isolated Afrikaner population was assessed with a battery of neuropsychological tests in an attempt to identify a BPD-associated quantitative trait or endophenotype. BPD individuals performed significantly worse than their unaffected relatives on visual and verbal memory tasks, a finding congruent with the literature. Afocused linkage and family-based association study was carried out using this memory-related endophenotype. In the largest 77-strong Afrikaner pedigree significant evidence for linkage was detected on chromosome 22q11, a region previously implicated in BPD. The quantitative transmission disequilibrium tests-based association analysis suggested that functional variants of the DRD4 and MAO-A genes modulate memory-related cognition. We speculate that polymorphisms at these loci may predispose to a subtype of BPD characterized by memory-related deficits.

Indexed as

FamilyGenetic LinkagePhenotypeBipolar DisorderChromosomes, Human, Pair 22Cohort StudiesGenetic Predisposition to DiseaseGenetic VariationGenotypeHumansNeuropsychological TestsPedigreeQuantitative Trait, HeritableSouth Africa

Identifiers

PMID17627031
OpenAlexW1986173814

What OpenQuestion holds

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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.