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Transcriptome-wide association study reveals two genes that influence mismatch negativity. 2021
Anjali Bhat, and
Haritz Irizar, and
Johan Hilge Thygesen, and
Karoline Kuchenbaecker, and
Oliver Pain, and
Rick A Adams, and
Eirini Zartaloudi, and
Jasmine Harju-Seppänen, and
Isabelle Austin-Zimmerman, and
Baihan Wang, and
Rebecca Muir, and
Ann Summerfelt, and
Xiaoming Michael Du, and
Heather Bruce, and
Patricio O'Donnell, and
Deepak P Srivastava, and
Karl Friston, and
L Elliot Hong, and
Mei-Hua Hall, and
Elvira Bramon
Division of Psychiatry, University College London, London, UK; Wellcome Centre for Human Neuroimaging, University College London, London, UK; Institute of Psychiatry, Psychology, and Neuroscience, King's College London, London, UK; Department of Basic and Clinical Neuroscience, Institute of Psychiatry, Psychology, and Neuroscience, King's College London, London, UK; MRC Centre for Neurodevelopmental Disorders, King's College London, London, UK. Electronic address: anjali.bhat.14@ucl.ac.uk.
Mismatch negativity (MMN) is a differential electrophysiological response measuring cortical adaptability to unpredictable stimuli. MMN is consistently attenuated in patients with psychosis. However, the genetics of MMN are uncharted, limiting the validation of MMN as a psychosis endophenotype. Here, we perform a transcriptome-wide association study of 728 individuals, which reveals 2 genes (FAM89A and ENGASE) whose expression in cortical tissues is associated with MMN. Enrichment analyses of neurodevelopmental expression signatures show that genes associated with MMN tend to be overexpressed in the frontal cortex during prenatal development but are significantly downregulated in adulthood. Endophenotype ranking value calculations comparing MMN and three other candidate psychosis endophenotypes (lateral ventricular volume and two auditory-verbal learning measures) find MMN to be considerably superior. These results yield promising insights into sensory processing in the cortex and endorse the notion of MMN as a psychosis endophenotype.
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