Evidence map›Paper›PMID 16391385›Full record

ReviewNeuromolecular medicine2005

Neurocognitive function as an endophenotype for genetic studies of bipolar affective disorder.

Jonathan B Savitz, Mark Solms, Rajkumar S Ramesar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neuromolecular medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

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

  1. Pooled it
  2. Trial
  3. Relations of gray matter volume to dimensional measures of cognition and affect in mood disorders.Cortex; a journal devoted to the study of the nervous system and behavior · 2022
    Article
  4. Article
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  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Intermediate: cognitive phenotypes in bipolar disorder.Journal of affective disorders · 2010
    Article
  13. Article
  14. Neurocognition in bipolar disorder and juvenile bipolar disorder.Journal of the Canadian Academy of Child and Adolescent Psychiatry = Journal de l'Academie canadienne de psychiatrie de l'enfant et de l'adolescent · 2009
    Article
  15. Article
  16. Article
  17. Multivariate genomewide linkage scan of neurocognitive traits and ADHD symptoms: suggestive linkage to 3q13.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2008
    Article
  18. Article
  19. Review
  20. 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.

Jonathan B SavitzMRC/UCT Human Genetics Research Unit, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Werner Beit North, Level 3, Faculty of Health Sciences, University of Cape Town, Observatory 7925, South Africa.
Mark Solms
Rajkumar S Ramesar

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The genetic basis of bipolar affective disorder remains opaque despite years of intensive investigation. One of the most serious difficulties for genetic research is the enormous phenotypic heterogeneity of psychiatric illnesses. As a response to this problem, geneticists have searched for alternative strategies to identify those individuals at genetic risk for developing the disorder. One approach is to use endophenotypes or intermediate traits. Gottesman and Gould (2003), in their discussion of endophenotypes, suggest five criteria that should be characteristic of a trait in order for it to qualify as an endophenotype. These five criteria are used in order to assess the viability of using measures of neuropsychological dysfunction as endophenotypes for genetic studies of bipolar disorder. A review of the literature suggests that executive dysfunction is characteristic of people with bipolar disorder in both the acute and chronic stages of the illness, that neurocognitive function is influenced by genetic factors and that neuropsychological deficits have been reported in the nonaffected relatives of bipolar probands. Nevertheless, it is unclear whether neuropsychological dysfunction co-segregates with affectively ill individuals. We conclude that the use of neurocognitive markers of bipolar illness suffers from a number of serious drawbacks but given the absence of more appropriate endophenotypes, the neuropsychological profiling of probands and their relatives may nevertheless prove to be a worthwhile exercise.

Indexed as

Genetic Predisposition to DiseasePhenotypeBipolar DisorderCognitionFamilyHumans

Identifiers

PMID16391385

What OpenQuestion holds

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Read underepoch 390

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.