Manuel Mattheisen

Genetics of response to cognitive behavior therapy in adults with major depression: a preliminary report

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  • Evelyn Andersson, Karolinska Institutet, Stockholm Water Co.
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  • James J. Crowley, Karolinska Institutet, The University of North Carolina at Chapel Hill, Department of Genetics, Chapel Hill, United States
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  • Nils Lindefors, Karolinska Institutet, Stockholm Water Co.
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  • Brjánn Ljótsson, Karolinska Institutet
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  • Erik Hedman-Lagerlöf, Karolinska Institutet
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  • Julia Boberg, Karolinska Institutet, Stockholm Water Co.
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  • Samir El Alaoui, Karolinska Institutet, Stockholm Water Co.
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  • Robert Karlsson, Karolinska Institutet
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  • Yi Lu, Karolinska Institutet
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  • Manuel Mattheisen
  • Anna K. Kähler, Karolinska Institutet
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  • Cecilia Svanborg, Karolinska Institutet, Stockholm Water Co.
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  • David Mataix-Cols, Karolinska Institutet, Stockholm Water Co.
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  • Simon Mattsson, Karolinska Institutet, Stockholm Water Co.
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  • Erik Forsell, Karolinska Institutet, Stockholm Water Co.
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  • Viktor Kaldo, Karolinska Institutet, Stockholm Water Co., Linnaeus University, Växjö
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  • Martin Schalling, Karolinska University Hospital
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  • Catharina Lavebratt, Karolinska University Hospital
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  • Patrick F. Sullivan, The University of North Carolina at Chapel Hill, Department of Genetics, Chapel Hill, United States, Karolinska Institutet
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  • Christian Rück, Karolinska Institutet, Stockholm Water Co.

Major depressive disorder is heritable and a leading cause of disability. Cognitive behavior therapy is an effective treatment for major depression. By quantifying genetic risk scores based on common genetic variants, the aim of this report was to explore the utility of psychiatric and cognitive trait genetic risk scores, for predicting the response of 894 adults with major depressive disorder to cognitive behavior therapy. The participants were recruited in a psychiatric setting, and the primary outcome score was measured using the Montgomery Åsberg Depression Rating Scale-Self Rated. Single-nucleotide polymorphism genotyping arrays were used to calculate the genomic risk scores based on large genetic studies of six phenotypes: major depressive disorder, bipolar disorder, attention-deficit/hyperactivity disorder, autism spectrum disorder, intelligence, and educational attainment. Linear mixed-effect models were used to test the relationships between the six genetic risk scores and cognitive behavior therapy outcome. Our analyses yielded one significant interaction effect (B = 0.09, p < 0.001): the autism spectrum disorder genetic risk score correlated with Montgomery Åsberg Depression Rating Scale-Self Rated changes during treatment, and the higher the autism spectrum disorder genetic load, the less the depressive symptoms decreased over time. The genetic risk scores for the other psychiatric and cognitive traits were not related to depressive symptom severity or change over time. Our preliminary results indicated, as expected, that the genomics of the response of patients with major depression to cognitive behavior therapy were complex and that future efforts should aim to maximize sample size and limit subject heterogeneity in order to gain a better understanding of the use of genetic risk factors to predict treatment outcome.

Original languageEnglish
JournalMolecular Psychiatry
Volume24
Issue4
Pages (from-to)484-490
Number of pages7
ISSN1359-4184
DOIs
Publication statusPublished - 2019

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