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Autoantibodies are not Predictive Markers for the Development of Depressive Symptoms in a Population-Based Cohort of Older Adults

Published online by Cambridge University Press:  15 July 2015

R.A. Iseme*
Affiliation:
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 CircuitNew Lambton Heights, 2305NSWAustralia
M. McEvoy
Affiliation:
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 CircuitNew Lambton Heights, 2305NSWAustralia
B. Kelly
Affiliation:
Centre for Translational Neuroscience and Mental Health Research, The University of Newcastle, Callaghan, NSWAustralia
L. Agnew
Affiliation:
Brain Behaviour Research Group, School of Science and Technology, University of New England, McClymont Building (W34) 353, Armidale, 2351NSWAustralia
J. Attia
Affiliation:
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 CircuitNew Lambton Heights, 2305NSWAustralia Division of Medicine, John Hunter Hospital, Lookout Road, New Lambton Heights, 2305NSWAustralia
F.R. Walker
Affiliation:
Laboratory of Affective Neuroscience, Medical Sciences MSB306, University of Newcastle, University Drive, Callaghan, 2308NSWAustralia
C. Oldmeadow
Affiliation:
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 CircuitNew Lambton Heights, 2305NSWAustralia
M. Boyle
Affiliation:
Division of Medicine, John Hunter Hospital, Lookout Road, New Lambton Heights, 2305NSWAustralia
*
*Corresponding author. Hunter Medical Research Institute Building, Level 3, Kookaburra Circuit, New Lambton Heights, NSW 2305, Australia. Tel.: +61 0403587865; fax: +61 2404220044. E-mail address: c3054392@uon.edu.au (R.A. Iseme).
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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.

Type
Original article
Copyright
Copyright © Elsevier Masson SAS 2015

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Footnotes

Abbreviations: CES-D, Centre for Epidemiological Study Depression; SLE, Systemic lupus erythematosus; ANA, Anti-nuclear autoantibodies; ENA, Extractable nuclear antigen autoantibodies; Sm, Anti-Smith; RNP, Ribo-nucleoprotein; SS-A, Sjogren's Syndrome A; SS-B, Sjogren's Syndrome B; SCL-70, Topoisomerase-I; JO-1, Autoantibodies against amino acyl-tRNA synthetases; IgG, Immunoglobulin G; IgA, Immunoglobulin A; ANCA, Anti-neutrophil cytoplasmic autoantibodies; TPO-Ab, Thyroid peroxidase autoantibodies; TTG-Ab, Tissue transglutaminase autoantibodies; ACGA, Anti-cardiolipin autoantibodies; RHF, Rheumatoid factor; CCP-Ab, Cyclic citrullinated peptide autoantibodies; hsCRP, High sensitivity C-reactive protein; DNA, Deoxyribonucleic acid; HCS, Hunter community study; LDL, Low-density lipoprotein; TGs, Triglycerides; BMI, Body Mass Index; PAL, Physical activity level; ARFS, Australian Recommended Food Score; FFQ, Food Frequency Questionnaire; DQESv2, Dietary Questionnaire for Epidemiological Studies version 2; AGHE, Australian Guide to Healthy Eating; ELISA, Enzyme-Linked Immunosorbent Assay; GPL, IgG phospholipid units; IU/mL, International unit per millilitre; EU/mL, Enzyme immunoassay units per millilitre; SD, Standard deviation; DAGs, Directed Acyclic Graphs; CNS, Central nervous system.

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