R A Iseme1, M McEvoy2, B Kelly3, L Agnew4, J Attia5, F R Walker6, C Oldmeadow2, M Boyle7. 1. Centre for Clinical Epidemiology and Biostatistics, Faculty of Health, School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute Building, Level 3, Kookaburra Circuit, New Lambton Heights, NSW 2305, Australia. Electronic address: c3054392@uon.edu.au. 2. Centre for Clinical Epidemiology and Biostatistics, Faculty of Health, School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute Building, Level 3, Kookaburra Circuit, New Lambton Heights, NSW 2305, Australia. 3. Centre for Translational Neuroscience and Mental Health Research, The University of Newcastle, Callaghan, NSW, Australia. 4. Brain Behaviour Research Group, School of Science and Technology, University of New England, McClymont Building (W34) 353, Armidale, NSW 2351, Australia. 5. Centre for Clinical Epidemiology and Biostatistics, Faculty of Health, School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia; Hunter Medical Research Institute Building, Level 3, Kookaburra Circuit, New Lambton Heights, NSW 2305, Australia; Division of Medicine, John Hunter Hospital, Lookout Road, New Lambton Heights, NSW 2305, Australia. 6. Laboratory of Affective Neuroscience, Medical Sciences MSB306, University of Newcastle, University Drive, Callaghan, NSW 2308, Australia. 7. Division of Medicine, John Hunter Hospital, Lookout Road, New Lambton Heights, NSW 2305, Australia.
Abstract
BACKGROUND: Autoantibodies have been implicated in the etiologic pathway of depressive disorders. Here, we determine the association between the presence of a panel of autoantibodies at baseline and change in depression symptom score over 5-year follow-up in a cohort of healthy elderly Australians. METHODS: Serum samples from 2049 randomly selected subjects enrolled in the Hunter Community Study (HCS) aged 55-85 years were assayed for a range of autoimmune markers (anti-nuclear autoantibodies, extractable nuclear antigen autoantibodies, anti-neutrophil cytoplasmic autoantibodies, thyroid peroxidase autoantibodies, tissue transglutaminase autoantibodies, anti-cardiolipin autoantibodies, rheumatoid factor and cyclic citrullinated peptide autoantibodies) at baseline. Depression symptom score was assessed using the Centre for Epidemiological Study (CES-D) scale at baseline and 5 years later. RESULTS: Autoantibody prevalence varied amongst our sample with ANA being the most prevalent; positive in 16% and borderline in 36% of study population. No evidence for a relationship was found between change in CES-D score over time and any autoimmune marker. Statins and high cholesterol were significantly associated with change in CES-D score over time in univariate analysis; however, these were probably confounded since they failed to remain significant following multivariable analysis. CONCLUSIONS: Autoantibodies were not associated with change in CES-D score over time. These findings point to an absence of autoimmune mechanisms in the general population or in moderate cases of depression.
BACKGROUND: Autoantibodies have been implicated in the etiologic pathway of depressive disorders. Here, we determine the association between the presence of a panel of autoantibodies at baseline and change in depression symptom score over 5-year follow-up in a cohort of healthy elderly Australians. METHODS: Serum samples from 2049 randomly selected subjects enrolled in the Hunter Community Study (HCS) aged 55-85 years were assayed for a range of autoimmune markers (anti-nuclear autoantibodies, extractable nuclear antigen autoantibodies, anti-neutrophil cytoplasmic autoantibodies, thyroid peroxidase autoantibodies, tissue transglutaminase autoantibodies, anti-cardiolipin autoantibodies, rheumatoid factor and cyclic citrullinated peptide autoantibodies) at baseline. Depression symptom score was assessed using the Centre for Epidemiological Study (CES-D) scale at baseline and 5 years later. RESULTS: Autoantibody prevalence varied amongst our sample with ANA being the most prevalent; positive in 16% and borderline in 36% of study population. No evidence for a relationship was found between change in CES-D score over time and any autoimmune marker. Statins and high cholesterol were significantly associated with change in CES-D score over time in univariate analysis; however, these were probably confounded since they failed to remain significant following multivariable analysis. CONCLUSIONS: Autoantibodies were not associated with change in CES-D score over time. These findings point to an absence of autoimmune mechanisms in the general population or in moderate cases of depression.