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Review
. 2022 Mar 2;13(3):457.
doi: 10.3390/genes13030457.

Genetic Predisposition to Schizophrenia and Depressive Disorder Comorbidity

Natalia A Shnayder  1   2 , Maxim A Novitsky  1 , Nikolay G Neznanov  1   3 , Oleg V Limankin  4   5   6 , Azat R Asadullin  7 , Artem V Petrov  2 , Diana V Dmitrenko  2 , Ekaterina A Narodova  2 , Natalia V Popenko  2 , Regina F Nasyrova  1   8
Affiliations
Review

Genetic Predisposition to Schizophrenia and Depressive Disorder Comorbidity

Natalia A Shnayder et al. Genes (Basel). .

Abstract

Background: Patients with schizophrenia have an increased risk of depressive disorders compared to the general population. The comorbidity between schizophrenia and depression suggests a potential coincidence of the pathophysiology and/or genetic predictors of these mental disorders. The aim of this study was to review the potential genetic predictors of schizophrenia and depression comorbidity. Materials and Methods: We carried out research and analysis of publications in the databases PubMed, Springer, Wiley Online Library, Taylor & Francis Online, Science Direct, and eLIBRARY.RU using keywords and their combinations. The search depth was the last 10 years (2010-2020). Full-text original articles, reviews, meta-analyses, and clinical observations were analyzed. A total of 459 articles were found, of which 45 articles corresponding to the purpose of this study were analyzed in this topic review. Results: Overlap in the symptoms and genetic predictors between these disorders suggests that a common etiological mechanism may underlie the presentation of comorbid depression in schizophrenia. The molecular mechanisms linking schizophrenia and depression are polygenic. The most studied candidate genes are GRIN1, GPM6A, SEPTIN4, TPH1, TPH2, CACNA1C, CACNB2, and BCL9.Conclusion: Planning and conducting genome-wide and associative genetic studies of the comorbid conditions under consideration in psychiatry is important for the development of biological and clinical predictors and a personalized therapy strategy for schizophrenia. However, it should be recognized that the problems of predictive and personalized psychiatry in the diagnosis and treatment of schizophrenia and comorbid disorders are far from being resolved.

Keywords: comorbidity; depression; genetics; pathophysiology; predictor; schizophrenia.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Venn diagram depicting the overlap of genes across schizophrenia and depression; pink color—schizophrenia genes; green color—depression genes; brown color—genes of schizophrenia and depression comorbidity.
Figure 2
Figure 2
The tissue expression of the glutamate ionotropic receptor NMDA type subunit 1 in the brain (a) and other organs in the human body (b).
Figure 3
Figure 3
The tissue expression of the protein M6A in the brain (a) and other organs in the human body (b).
Figure 4
Figure 4
The tissue expression of the septin type 4 in the brain (a) and other organs in the human body (b).
Figure 5
Figure 5
The tissue expression of tryptophan hydroxylase type 1 in the brain (a) and other organs in the human body (b).
Figure 6
Figure 6
The tissue expression of the tryptophan hydroxylase type 2 in the brain (a) and other organs in the human body (b).
Figure 7
Figure 7
The tissue expression of calcium voltage-gated channel subunit alpha1 C in the brain (a) and other organs in the human body (b).
Figure 8
Figure 8
The tissue expression of the calcium voltage-gated channel auxiliary subunit β 2 in the brain (a) and other organs in the human body (b).
Figure 9
Figure 9
The tissue expression of the BCL6 transcription repressor in the brain (a) and other organs in the human body (b).
See this image and copyright information in PMC

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References

    1. Ekman M., Granström O., Omerov S., Jacob J., Landén M. The Societal Cost of Schizophrenia in Sweden. J. Ment. Health Policy Econ. 2013;16:13–25. doi: 10.1016/S1098-3015(10)72536-5. - DOI - PubMed
    1. World Health Organization . The Global Burden of Disease: 2004 Update. World Health Organization; Geneva, Switzerland: 2008.
    1. Whiteford H.A., Degenhardt L., Rehm J., Baxter A.J., Ferrari A.J., Erskine H.E., Charlson F.J., Norman R.E., Flaxman A.D., Johns N., et al. Global burden of disease attributable to mental and substance use disorders: Findings from the Global Burden of Disease Study 2010. Lancet. 2013;382:1575–1586. doi: 10.1016/S0140-6736(13)61611-6. - DOI - PubMed
    1. Buckley P.F., Miller B.J., Lehrer D., Castle D.J. Psychiatric Comorbidities and Schizophrenia. Schizophr. Bull. 2008;35:383–402. doi: 10.1093/schbul/sbn135. - DOI - PMC - PubMed
    1. Häfner H., Maurer K., der Heiden W.A. Schizophrenia—A disorder in its own right? Results from 25 years of the ABC study. Nervenarzt. 2013;84:1093–1103. doi: 10.1007/s00115-013-3788-6. - DOI - PubMed

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