The impact of genetic variations in the serotonergic system on symptom severity and clinical outcome in functional neurological disorders
We studied gene-environment, as well as gene-gene interaction to elucidate their effects on symptom severity and predict clinical outcomes in functional neurological disorders (FND). Eighty-five patients with mixed FND were genotyped for ten single-nucleotide polymorphisms (SNP) from seven different...
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Published in | Journal of psychosomatic research Vol. 186; p. 111909 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.11.2024
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Abstract | We studied gene-environment, as well as gene-gene interaction to elucidate their effects on symptom severity and predict clinical outcomes in functional neurological disorders (FND).
Eighty-five patients with mixed FND were genotyped for ten single-nucleotide polymorphisms (SNP) from seven different stress-related genes. We tested cross-sectionally the association between genotype and the symptomatology of FND (symptom severity assessed with the examiner-based clinical global impression score [CGI] and age of onset). Clinical outcome was assessed in 52 patients who participated in a follow-up clinical visit after eight months (following their individual therapies as usual). We tested longitudinally the association between genotype and clinical outcome in FND. We examined the contribution of each SNP and their interaction between them to FND symptomatology and outcome.
We identified a nominal association between tryptophan hydroxylase 1 (TPH1) rs1800532 and symptom severity (CGI1) in FND under a codominant model (T/T: ßT/T = 2.31, seT/T = 0.57; G/T: ßG/T = -0.18, seG/T = 0.29, P = 0.035), with minor allele (T) carriers presenting more severe symptoms. An association was identified between TPH1 and clinical outcome, suggesting that major allele (G) carriers were more likely to have an improved outcome under a codominant model (G/T: ORG/T = 0.18, CIG/T = [0.02–1.34]; T/T: ORT/T = 2.08, CIT/T = [0.30–14.53], P = 0.041). Our analyses suggested a significant gene-gene interaction for TPH2 (rs4570625) and OXTR (rs2254298) on symptom severity, and a significant gene-gene interaction for TPH1, TPH2 and BDNF (rs1491850) on clinical outcome.
FND might arise from a complex interplay between individual predisposing risk genes involved in the serotonergic pathway and their gene-gene interactions.
•A nominal association was found between clinical outcome and TPH1 variant.•A TPH2 and OXTR gene-gene interaction might modulate symptom severity.•TPH1, TPH2 and BDNF gene-gene interaction might modulate clinical outcome. |
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AbstractList | We studied gene-environment, as well as gene-gene interaction to elucidate their effects on symptom severity and predict clinical outcomes in functional neurological disorders (FND).OBJECTIVEWe studied gene-environment, as well as gene-gene interaction to elucidate their effects on symptom severity and predict clinical outcomes in functional neurological disorders (FND).Eighty-five patients with mixed FND were genotyped for ten single-nucleotide polymorphisms (SNP) from seven different stress-related genes. We tested cross-sectionally the association between genotype and the symptomatology of FND (symptom severity assessed with the examiner-based clinical global impression score [CGI] and age of onset). Clinical outcome was assessed in 52 patients who participated in a follow-up clinical visit after eight months (following their individual therapies as usual). We tested longitudinally the association between genotype and clinical outcome in FND. We examined the contribution of each SNP and their interaction between them to FND symptomatology and outcome.METHODSEighty-five patients with mixed FND were genotyped for ten single-nucleotide polymorphisms (SNP) from seven different stress-related genes. We tested cross-sectionally the association between genotype and the symptomatology of FND (symptom severity assessed with the examiner-based clinical global impression score [CGI] and age of onset). Clinical outcome was assessed in 52 patients who participated in a follow-up clinical visit after eight months (following their individual therapies as usual). We tested longitudinally the association between genotype and clinical outcome in FND. We examined the contribution of each SNP and their interaction between them to FND symptomatology and outcome.We identified a nominal association between tryptophan hydroxylase 1 (TPH1) rs1800532 and symptom severity (CGI1) in FND under a codominant model (T/T: ßT/T = 2.31, seT/T = 0.57; G/T: ßG/T = -0.18, seG/T = 0.29, P = 0.035), with minor allele (T) carriers presenting more severe symptoms. An association was identified between TPH1 and clinical outcome, suggesting that major allele (G) carriers were more likely to have an improved outcome under a codominant model (G/T: ORG/T = 0.18, CIG/T = [0.02-1.34]; T/T: ORT/T = 2.08, CIT/T = [0.30-14.53], P = 0.041). Our analyses suggested a significant gene-gene interaction for TPH2 (rs4570625) and OXTR (rs2254298) on symptom severity, and a significant gene-gene interaction for TPH1, TPH2 and BDNF (rs1491850) on clinical outcome.RESULTSWe identified a nominal association between tryptophan hydroxylase 1 (TPH1) rs1800532 and symptom severity (CGI1) in FND under a codominant model (T/T: ßT/T = 2.31, seT/T = 0.57; G/T: ßG/T = -0.18, seG/T = 0.29, P = 0.035), with minor allele (T) carriers presenting more severe symptoms. An association was identified between TPH1 and clinical outcome, suggesting that major allele (G) carriers were more likely to have an improved outcome under a codominant model (G/T: ORG/T = 0.18, CIG/T = [0.02-1.34]; T/T: ORT/T = 2.08, CIT/T = [0.30-14.53], P = 0.041). Our analyses suggested a significant gene-gene interaction for TPH2 (rs4570625) and OXTR (rs2254298) on symptom severity, and a significant gene-gene interaction for TPH1, TPH2 and BDNF (rs1491850) on clinical outcome.FND might arise from a complex interplay between individual predisposing risk genes involved in the serotonergic pathway and their gene-gene interactions.CONCLUSIONFND might arise from a complex interplay between individual predisposing risk genes involved in the serotonergic pathway and their gene-gene interactions. We studied gene-environment, as well as gene-gene interaction to elucidate their effects on symptom severity and predict clinical outcomes in functional neurological disorders (FND). Eighty-five patients with mixed FND were genotyped for ten single-nucleotide polymorphisms (SNP) from seven different stress-related genes. We tested cross-sectionally the association between genotype and the symptomatology of FND (symptom severity assessed with the examiner-based clinical global impression score [CGI] and age of onset). Clinical outcome was assessed in 52 patients who participated in a follow-up clinical visit after eight months (following their individual therapies as usual). We tested longitudinally the association between genotype and clinical outcome in FND. We examined the contribution of each SNP and their interaction between them to FND symptomatology and outcome. We identified a nominal association between tryptophan hydroxylase 1 (TPH1) rs1800532 and symptom severity (CGI ) in FND under a codominant model (T/T: ß = 2.31, se = 0.57; G/T: ß = -0.18, se = 0.29, P = 0.035), with minor allele (T) carriers presenting more severe symptoms. An association was identified between TPH1 and clinical outcome, suggesting that major allele (G) carriers were more likely to have an improved outcome under a codominant model (G/T: OR = 0.18, CI = [0.02-1.34]; T/T: OR = 2.08, CI = [0.30-14.53], P = 0.041). Our analyses suggested a significant gene-gene interaction for TPH2 (rs4570625) and OXTR (rs2254298) on symptom severity, and a significant gene-gene interaction for TPH1, TPH2 and BDNF (rs1491850) on clinical outcome. FND might arise from a complex interplay between individual predisposing risk genes involved in the serotonergic pathway and their gene-gene interactions. We studied gene-environment, as well as gene-gene interaction to elucidate their effects on symptom severity and predict clinical outcomes in functional neurological disorders (FND). Eighty-five patients with mixed FND were genotyped for ten single-nucleotide polymorphisms (SNP) from seven different stress-related genes. We tested cross-sectionally the association between genotype and the symptomatology of FND (symptom severity assessed with the examiner-based clinical global impression score [CGI] and age of onset). Clinical outcome was assessed in 52 patients who participated in a follow-up clinical visit after eight months (following their individual therapies as usual). We tested longitudinally the association between genotype and clinical outcome in FND. We examined the contribution of each SNP and their interaction between them to FND symptomatology and outcome. We identified a nominal association between tryptophan hydroxylase 1 (TPH1) rs1800532 and symptom severity (CGI1) in FND under a codominant model (T/T: ßT/T = 2.31, seT/T = 0.57; G/T: ßG/T = -0.18, seG/T = 0.29, P = 0.035), with minor allele (T) carriers presenting more severe symptoms. An association was identified between TPH1 and clinical outcome, suggesting that major allele (G) carriers were more likely to have an improved outcome under a codominant model (G/T: ORG/T = 0.18, CIG/T = [0.02–1.34]; T/T: ORT/T = 2.08, CIT/T = [0.30–14.53], P = 0.041). Our analyses suggested a significant gene-gene interaction for TPH2 (rs4570625) and OXTR (rs2254298) on symptom severity, and a significant gene-gene interaction for TPH1, TPH2 and BDNF (rs1491850) on clinical outcome. FND might arise from a complex interplay between individual predisposing risk genes involved in the serotonergic pathway and their gene-gene interactions. •A nominal association was found between clinical outcome and TPH1 variant.•A TPH2 and OXTR gene-gene interaction might modulate symptom severity.•TPH1, TPH2 and BDNF gene-gene interaction might modulate clinical outcome. |
ArticleNumber | 111909 |
Author | Rey Álvarez, Lucía Trinidad Ansede-Bermejo, Juan Bühler, Janine Aybek, Selma del Real, Álvaro Weber, Samantha Carracedo, Ángel Cruz, Raquel |
Author_xml | – sequence: 1 givenname: Samantha surname: Weber fullname: Weber, Samantha organization: Department of Neurology, Psychosomatic Medicine Unit, Inselspital Bern University Hospital, University of Bern, 3012 Bern, Switzerland – sequence: 2 givenname: Lucía Trinidad surname: Rey Álvarez fullname: Rey Álvarez, Lucía Trinidad organization: Department of Neurology, Psychosomatic Medicine Unit, Inselspital Bern University Hospital, University of Bern, 3012 Bern, Switzerland – sequence: 3 givenname: Juan surname: Ansede-Bermejo fullname: Ansede-Bermejo, Juan organization: Centro Nacional de Genotipado (CEGEN), Universidade de Santiago de Compostela, Santiago de Compostela, Spain – sequence: 4 givenname: Raquel surname: Cruz fullname: Cruz, Raquel organization: Centro Nacional de Genotipado (CEGEN), Universidade de Santiago de Compostela, Santiago de Compostela, Spain – sequence: 5 givenname: Álvaro surname: del Real fullname: del Real, Álvaro organization: Medicine and Psychiatry Department, University of Cantabria, Santander, Spain – sequence: 6 givenname: Janine surname: Bühler fullname: Bühler, Janine organization: Department of Neurology, Psychosomatic Medicine Unit, Inselspital Bern University Hospital, University of Bern, 3012 Bern, Switzerland – sequence: 7 givenname: Ángel surname: Carracedo fullname: Carracedo, Ángel organization: Centro Nacional de Genotipado (CEGEN), Universidade de Santiago de Compostela, Santiago de Compostela, Spain – sequence: 8 givenname: Selma surname: Aybek fullname: Aybek, Selma email: selma.aybek@unifr.ch organization: Department of Neurology, Psychosomatic Medicine Unit, Inselspital Bern University Hospital, University of Bern, 3012 Bern, Switzerland |
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Keywords | Neural plasticity OXTR Serotonin BDNF Conversion disorders TPH Stress |
Language | English |
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4 Gonzalez (10.1016/j.jpsychores.2024.111909_bb0140) 2007; 23 Weber (10.1016/j.jpsychores.2024.111909_bb0060) 2022 Motsinger (10.1016/j.jpsychores.2024.111909_bb0150) 2006; 2 Asadi-Pooya (10.1016/j.jpsychores.2024.111909_bb0040) 2023; 8 Real (10.1016/j.jpsychores.2024.111909_bb0215) 2009; 66 Wilson (10.1016/j.jpsychores.2024.111909_bb0170) 2012; 22 Lugo-Huitrón (10.1016/j.jpsychores.2024.111909_bb0185) 2011; 33 Furmark (10.1016/j.jpsychores.2024.111909_bb0225) 2008; 28 Djalali (10.1016/j.jpsychores.2024.111909_bb0210) 2005; 92 Keynejad (10.1016/j.jpsychores.2024.111909_bb0055) 2019; 90 Schneider (10.1016/j.jpsychores.2024.111909_bb0080) 2024; 43 Womersley (10.1016/j.jpsychores.2024.111909_bb0120) 2020; 21 Moskaleva (10.1016/j.jpsychores.2024.111909_bb0155) 2022; 52 |
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SubjectTerms | Adult Aged BDNF Conversion disorders Cross-Sectional Studies Female Gene-Environment Interaction Genotype Humans Male Middle Aged Nervous System Diseases - genetics Neural plasticity OXTR Polymorphism, Single Nucleotide - genetics Serotonin Severity of Illness Index Stress TPH Tryptophan Hydroxylase - genetics |
Title | The impact of genetic variations in the serotonergic system on symptom severity and clinical outcome in functional neurological disorders |
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