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Considering medication exposure in genomic association studies of cognition in psychotic disorders

    Seenae Eum

    *Author for correspondence:

    E-mail Address: seum@su.edu

    Department of Pharmacogenomics, School of Pharmacy, Shenandoah University, Fairfax, VA 22031, USA

    ,
    Scot Kristian Hill

    Department of Psychology, Rosalind Franklin University of Medicine & Science, North Chicago, IL 60064, USA

    &
    Jeffrey R Bishop

    Department of Experimental & Clinical Pharmacology, College of Pharmacy, University of Minnesota, Minneapolis, MN 55455, USA

    Department of Psychiatry & Behavioral Sciences, University of Minnesota Medical School, Minneapolis, MN 55455, USA

    Published Online:https://doi.org/10.2217/pgs-2022-0070

    Cognitive dysfunction is a core feature of psychosis-spectrum illnesses, and the characterization of related genetic mechanisms may provide insights regarding the disease pathophysiology. Substantial efforts have been made to determine the genetic component of cognitive symptoms, without clear success. Illness-related moderators and environmental factors such as medications hinder the detection of genomic association with cognition. Polypharmacy is common in psychotic disorders, and the cumulative effects of medication regimens can confound gene–cognition associations. A review of the relative contributions of important pharmacological and genetic relationships identifies that the effects of medications on cognition in psychotic disorders may be at least, if not more, impactful than individual genes, thus underscoring the importance of accounting for medication exposure in gene–cognition association studies.

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