Evidence map›Paper›PMID 40254710›Full record

ArticleMolecular psychiatry2025

Exploring the implications of case selection methods for psychiatric molecular genetic studies.

Kenneth S Kendler, Henrik Ohlsson, Jan Sundquist, Kristina Sundquist

Abstract read
In one paragraph

Article in Molecular psychiatry, 2025. 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
–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

1 citing paper in PubMed.

  1. Review
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.

Kenneth S KendlerVirginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA. Kenneth.Kendler@vcuhealth.org.ORCID 0000-0001-8689-6570
Henrik OhlssonCenter for Primary Health Care Research, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Jan SundquistCenter for Primary Health Care Research, Department of Clinical Sciences, Lund University, Malmö, Sweden.ORCID 0000-0001-7228-5015
Kristina SundquistCenter for Primary Health Care Research, Department of Clinical Sciences, Lund University, Malmö, Sweden.

Funding

Genetic, Social, and Developmental Epidemiology of Drug Use DisordersR01DA030005 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI KENNETH SEEDMAN KENDLER, JAN O SUNDQUIST · 2010 to 2026
$7.6M
Social, Developmental and Genetic Epidemiology of Alcohol Use DisordersR01AA023534 · NIAAA · VIRGINIA COMMONWEALTH UNIVERSITY · PI KENDLER, KENNETH SEEDMAN, SUNDQUIST, KRISTINA · 2015 to 2023
$4.0M
NIAAA NIH HHS R01 AA023534NIDA NIH HHS R01 DA030005U.S. Department of Health & Human Services | NIH | National Institute on Alcohol Abuse and Alcoholism (NIAAA) R01AA023534U.S. Department of Health & Human Services | NIH | National Institute on Drug Abuse (NIDA) R01DA030005Vetenskapsrådet (Swedish Research Council) 2020-01175Vetenskapsrådet (Swedish Research Council) 2021-06467
6 · The paper itself

Abstract

Researchers selecting probands for molecular genetic studies confront a range of sampling issues with modest empirical guidance. In this paper, using cases of major depression (MD), anxiety disorders (AD) alcohol use disorder (AUD), drug use disorder (DUD), bipolar disorder (BD) and schizophrenia (SZ) from a large population cohort of all native Swedes born 1940-2003, we examine the implications of three proband selection decisions by exploring profiles of genetic risks assessed using the validated family genetic risk scores. The impact of censoring cases with comorbid diagnoses is quite variable, depending on the frequency of that disorder in the case sample and the genetic relationship of the censored to the primary disorder. In an MD cohort, censoring SZ cases produces only a focal small decrease in schizophrenia genetic risk while censoring AD cases produces a wide-spread reduction in genetic risk for MD and most other disorders. We examine the value of censoring cases of SZ, BD and MD whose onset was preceded by one to two years by first episodes of DUD or AUD. We do not see any increase in genetic risk for these "screened" cohorts. Secondary ascertainment, where disorder A is ascertained as a comorbid diagnosis in a sample collected for disorder B, can, in certain situations, produces large increases in the genetic risk for disorder B and associated disorders in cases of A. However, if disorder B is closely genetically related to disorder A (as seen with MD/AD and DUD/AUD pairings), the pattern differs dramatically and produces a general moderate elevation across the genetic risk profile. These findings provide guidelines for future investigators and suggest caution when screening out comorbid disorders and when utilizing secondary ascertainment.

Indexed as

Genetic Predisposition to DiseaseMental DisordersPatient SelectionAdultBipolar DisorderCohort StudiesComorbidityFemaleHumansMajor Depressive DisorderMaleMiddle AgedSchizophreniaSubstance-Related Disorders

Identifiers

PMID40254710
PMCPMC12339360

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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.