Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder
Abstract Epigenetic modifications occur sequentially during the lifespan, but their pace can be altered by external stimuli. The onset of schizophrenia and bipolar disorder is critically modulated by stressors that may alter the epigenetic pattern, a putative signature marker of exposure to environm...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2023-05-01
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| Series: | Translational Psychiatry |
| Online Access: | https://doi.org/10.1038/s41398-023-02463-w |
| _version_ | 1797827316135493632 |
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| author | Alex G. Segura Elena de la Serna Gisela Sugranyes Inmaculada Baeza Isabel Valli Covadonga Díaz-Caneja Nuria Martín Dolores M. Moreno Patricia Gassó Natalia Rodriguez Sergi Mas Josefina Castro-Fornieles |
| author_facet | Alex G. Segura Elena de la Serna Gisela Sugranyes Inmaculada Baeza Isabel Valli Covadonga Díaz-Caneja Nuria Martín Dolores M. Moreno Patricia Gassó Natalia Rodriguez Sergi Mas Josefina Castro-Fornieles |
| author_sort | Alex G. Segura |
| collection | DOAJ |
| description | Abstract Epigenetic modifications occur sequentially during the lifespan, but their pace can be altered by external stimuli. The onset of schizophrenia and bipolar disorder is critically modulated by stressors that may alter the epigenetic pattern, a putative signature marker of exposure to environmental risk factors. In this study, we estimated the age-related epigenetic modifications to assess the differences between young individuals at familial high risk (FHR) and controls and their association with environmental stressors. The sample included 117 individuals (6–17 years) at FHR (45%) and a control group (55%). Blood and saliva samples were used estimate the epigenetic age with six epigenetic clocks through methylation data. Environmental risk was measured with obstetric complications, socioeconomic statuses and recent stressful life events data. Epigenetic age was correlated with chronological age. FHR individuals showed epigenetic age deacceleration of Horvath and Hannum epigenetic clocks compared to controls. No effect of the environmental risk factors on the epigenetic age acceleration could be detected. Epigenetic age acceleration adjusted by cell counts showed that the FHR group was deaccelerated also with the PedBE epigenetic clock. Epigenetic age asynchronicities were found in the young at high risk, suggesting that offspring of affected parents follow a slower pace of biological aging than the control group. It still remains unclear which environmental stressors orchestrate the changes in the methylation pattern. Further studies are needed to better characterize the molecular impact of environmental stressors before illness onset, which could be critical in the development of tools for personalized psychiatry. |
| first_indexed | 2024-04-09T12:45:53Z |
| format | Article |
| id | doaj.art-14368d4819234db8b2887e95555b666c |
| institution | Directory Open Access Journal |
| issn | 2158-3188 |
| language | English |
| last_indexed | 2024-04-09T12:45:53Z |
| publishDate | 2023-05-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Translational Psychiatry |
| spelling | doaj.art-14368d4819234db8b2887e95555b666c2023-05-14T11:28:42ZengNature Publishing GroupTranslational Psychiatry2158-31882023-05-011311810.1038/s41398-023-02463-wEpigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorderAlex G. Segura0Elena de la Serna1Gisela Sugranyes2Inmaculada Baeza3Isabel Valli4Covadonga Díaz-Caneja5Nuria Martín6Dolores M. Moreno7Patricia Gassó8Natalia Rodriguez9Sergi Mas10Josefina Castro-Fornieles11Department of Clinical Foundations, Pharmacology Unit, University of BarcelonaChild and Adolescent Psychiatry and Psychology Department, 2021SGR01319, Institute of Neuroscience, Hospital Clínic de BarcelonaChild and Adolescent Psychiatry and Psychology Department, 2021SGR01319, Institute of Neuroscience, Hospital Clínic de BarcelonaChild and Adolescent Psychiatry and Psychology Department, 2021SGR01319, Institute of Neuroscience, Hospital Clínic de BarcelonaInstitut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM)Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM)Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM)Department of Clinical Foundations, Pharmacology Unit, University of BarcelonaDepartment of Clinical Foundations, Pharmacology Unit, University of BarcelonaDepartment of Clinical Foundations, Pharmacology Unit, University of BarcelonaChild and Adolescent Psychiatry and Psychology Department, 2021SGR01319, Institute of Neuroscience, Hospital Clínic de BarcelonaAbstract Epigenetic modifications occur sequentially during the lifespan, but their pace can be altered by external stimuli. The onset of schizophrenia and bipolar disorder is critically modulated by stressors that may alter the epigenetic pattern, a putative signature marker of exposure to environmental risk factors. In this study, we estimated the age-related epigenetic modifications to assess the differences between young individuals at familial high risk (FHR) and controls and their association with environmental stressors. The sample included 117 individuals (6–17 years) at FHR (45%) and a control group (55%). Blood and saliva samples were used estimate the epigenetic age with six epigenetic clocks through methylation data. Environmental risk was measured with obstetric complications, socioeconomic statuses and recent stressful life events data. Epigenetic age was correlated with chronological age. FHR individuals showed epigenetic age deacceleration of Horvath and Hannum epigenetic clocks compared to controls. No effect of the environmental risk factors on the epigenetic age acceleration could be detected. Epigenetic age acceleration adjusted by cell counts showed that the FHR group was deaccelerated also with the PedBE epigenetic clock. Epigenetic age asynchronicities were found in the young at high risk, suggesting that offspring of affected parents follow a slower pace of biological aging than the control group. It still remains unclear which environmental stressors orchestrate the changes in the methylation pattern. Further studies are needed to better characterize the molecular impact of environmental stressors before illness onset, which could be critical in the development of tools for personalized psychiatry.https://doi.org/10.1038/s41398-023-02463-w |
| spellingShingle | Alex G. Segura Elena de la Serna Gisela Sugranyes Inmaculada Baeza Isabel Valli Covadonga Díaz-Caneja Nuria Martín Dolores M. Moreno Patricia Gassó Natalia Rodriguez Sergi Mas Josefina Castro-Fornieles Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder Translational Psychiatry |
| title | Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder |
| title_full | Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder |
| title_fullStr | Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder |
| title_full_unstemmed | Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder |
| title_short | Epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder |
| title_sort | epigenetic age deacceleration in youth at familial risk for schizophrenia and bipolar disorder |
| url | https://doi.org/10.1038/s41398-023-02463-w |
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