Ana Marta Ferreira1, Bárbara Leal2, Inês Ferreira3, Sandra Brás4, Inês Moreira5, Raquel Samões6, Ana Paula Sousa7, Ernestina Santos8, Berta Silva9, Paulo Pinho Costa10, Sara Cavaco11, Ana Martins da Silva12. 1. Laboratório de Imunogenética, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal; Unidade Multidisciplinar de Investigação Biomédica, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal. Electronic address: anamartapdf@gmail.com. 2. Laboratório de Imunogenética, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal; Unidade Multidisciplinar de Investigação Biomédica, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal. Electronic address: baguerraleal@gmail.com. 3. Unidade de Neuropsicologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: inesalmeida@ua.pt. 4. Laboratório de Imunogenética, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal. Electronic address: sfmaia@icbas.up.pt. 5. Unidade de Neuropsicologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: inesmoreira.ae@gmail.com. 6. Serviço de Neurologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: raquelsamoes.neurologia@chporto.min-saude.pt. 7. Serviço de Neurofisiologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: apdiogosousa@gmail.com. 8. Serviço de Neurologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal; Serviço de Neurofisiologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: ernestinasantos.neurologia@chporto.min-saude.pt. 9. Laboratório de Imunogenética, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal; Unidade Multidisciplinar de Investigação Biomédica, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal. Electronic address: bertams@icbas.up.pt. 10. Laboratório de Imunogenética, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal; Unidade Multidisciplinar de Investigação Biomédica, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal; Departamento de Genética Humana, Instituto Nacional de Saúde Dr. Ricardo Jorge - Porto, Portugal. Electronic address: paulo.costa@insa.min-saude.pt. 11. Unidade de Neuropsicologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: saramscavaco@gmail.com. 12. Unidade Multidisciplinar de Investigação Biomédica, Instituto de Ciências Biomédicas Abel Salazar - Universidade do Porto, Portugal; Serviço de Neurologia, Centro Hospitalar Universitário do Porto - Hospital de Santo António, Portugal. Electronic address: anamartins.neurologia@chporto.min-saude.pt.
Abstract
BACKGROUND: Mood disorders, as depression and anxiety, are frequent in Multiple Sclerosis (MS) patients. High pro-inflammatory cytokine levels (e.g. IL-1β) have been reported in depressed individuals. OBJECTIVE: We aimed to investigate the role of the rs16944 (IL-1β-511 C>T) polymorphism in the development of anxiety and depression symptoms in a Portuguese cohort of MS patients. METHODS: 393 MS patients answered the Hospital Anxiety and Depression Scale (HADS) at T1. This questionnaire was reapplied to a subgroup of 175 MS patients approximately three years later (T2). HADS cut-off scores for anxiety and depression were respectively ≥11 and ≥8. RESULTS: At T1, anxiety was found in 106 MS patients (27.0%) and 11 controls (16.7%); whereas depression was identified in 116 (29.5%) MS patients and 9 controls (13.6%). Persistent anxiety and depression were respectively recorded in 12% and 20% of MS patients. The rs16944TT genotype was found to be a susceptibility factor for the occurrence of depression at T1 (OR = 3.16, p=0.002) and the development of persistent depression (OR = 5.63, p=0.003) in MS. CONCLUSION: Study results support the hypothesis that inflammation is a significant factor in psychopathology development.
BACKGROUND: Mood disorders, as depression and anxiety, are frequent in Multiple Sclerosis (MS) patients. High pro-inflammatory cytokine levels (e.g. IL-1β) have been reported in depressed individuals. OBJECTIVE: We aimed to investigate the role of the rs16944 (IL-1β-511 C>T) polymorphism in the development of anxiety and depression symptoms in a Portuguese cohort of MS patients. METHODS: 393 MS patients answered the Hospital Anxiety and Depression Scale (HADS) at T1. This questionnaire was reapplied to a subgroup of 175 MS patients approximately three years later (T2). HADS cut-off scores for anxiety and depression were respectively ≥11 and ≥8. RESULTS: At T1, anxiety was found in 106 MS patients (27.0%) and 11 controls (16.7%); whereas depression was identified in 116 (29.5%) MS patients and 9 controls (13.6%). Persistent anxiety and depression were respectively recorded in 12% and 20% of MS patients. The rs16944TT genotype was found to be a susceptibility factor for the occurrence of depression at T1 (OR = 3.16, p=0.002) and the development of persistent depression (OR = 5.63, p=0.003) in MS. CONCLUSION: Study results support the hypothesis that inflammation is a significant factor in psychopathology development.