Sex-specific transcriptional and proteomic signatures in schizophrenia

Jari Tiihonen (), Marja Koskuvi, Markus Storvik, Ida Hyötyläinen, Yanyan Gao, Katja A. Puttonen, Raisa Giniatullina, Ekaterina Poguzhelskaya, Ilkka Ojansuu, Olli Vaurio, Tyrone D. Cannon, Jouko Lönnqvist, Sebastian Therman, Jaana Suvisaari, Jaakko Kaprio, Lesley Cheng, Andrew F. Hill, Markku Lähteenvuo, Jussi Tohka, Rashid Giniatullin, Šárka Lehtonen () and Jari Koistinaho ()
Additional contact information
Jari Tiihonen: Karolinska Institutet
Marja Koskuvi: University of Eastern Finland
Markus Storvik: University of Eastern Finland
Ida Hyötyläinen: University of Eastern Finland
Yanyan Gao: University of Eastern Finland
Katja A. Puttonen: University of Eastern Finland
Raisa Giniatullina: University of Eastern Finland
Ekaterina Poguzhelskaya: University of Eastern Finland
Ilkka Ojansuu: University of Eastern Finland, Niuvanniemi Hospital
Olli Vaurio: University of Eastern Finland, Niuvanniemi Hospital
Tyrone D. Cannon: Yale University
Jouko Lönnqvist: National Institute for Health and Welfare
Sebastian Therman: National Institute for Health and Welfare
Jaana Suvisaari: National Institute for Health and Welfare
Jaakko Kaprio: University of Helsinki
Lesley Cheng: La Trobe University
Andrew F. Hill: La Trobe University
Markku Lähteenvuo: University of Eastern Finland, Niuvanniemi Hospital
Jussi Tohka: University of Eastern Finland
Rashid Giniatullin: University of Eastern Finland
Šárka Lehtonen: University of Eastern Finland
Jari Koistinaho: University of Eastern Finland

Nature Communications, 2019, vol. 10, issue 1, 1-11

Abstract: Abstract It has remained unclear why schizophrenia typically manifests after adolescence and which neurobiological mechanisms are underlying the cascade leading to the actual onset of the illness. Here we show that the use of induced pluripotent stem cell-derived neurons of monozygotic twins from pairs discordant for schizophrenia enhances disease-specific signal by minimizing genetic heterogeneity. In proteomic and pathway analyses, clinical illness is associated especially with altered glycosaminoglycan, GABAergic synapse, sialylation, and purine metabolism pathways. Although only 12% of all 19,462 genes are expressed differentially between healthy males and females, up to 61% of the illness-related genes are sex specific. These results on sex-specific genes are replicated in another dataset. This implies that the pathophysiology differs between males and females, and may explain why symptoms appear after adolescence when the expression of many sex-specific genes change, and suggests the need for sex-specific treatments.

Date: 2019
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DOI: 10.1038/s41467-019-11797-3

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