Yann Quidé1, Chiara C Bortolasci2, Briana Spolding2, Srisaiyini Kidnapillai2, Oliver J Watkeys3, Sarah Cohen-Woods4, Vaughan J Carr5, Michael Berk6, Ken Walder7, Melissa J Green3. 1. School of Psychiatry, University of New South Wales (UNSW), Sydney, NSW, Australia; Neuroscience Research Australia, Randwick, NSW, Australia. Electronic address: y.quide@unsw.edu.au. 2. Centre for Molecular and Medical Research, School of Medicine, Deakin University, Geelong, VIC, Australia. 3. School of Psychiatry, University of New South Wales (UNSW), Sydney, NSW, Australia; Neuroscience Research Australia, Randwick, NSW, Australia. 4. Discipline of Psychology, Flinders University, Adelaide, SA, Australia; Flinders Centre for Innovation in Cancer, Adelaide, SA, Australia; Órama Institute, College of Education, Psychology, and Social Work, Flinders University, Adelaide, SA, Australia. 5. School of Psychiatry, University of New South Wales (UNSW), Sydney, NSW, Australia; Neuroscience Research Australia, Randwick, NSW, Australia; Department of Psychiatry, School of Clinical Sciences, Monash University, Clayton, VIC, Australia. 6. Centre for Molecular and Medical Research, School of Medicine, Deakin University, Geelong, VIC, Australia; Deakin University, IMPACT, the Institute for Mental and Physical Health and Clinical Translation, Barwon Health, Geelong, VIC, Australia; Florey Institute for Neuroscience and Mental Health, Parkville, VIC, Australia; Orygen, The National Centre of Excellence in Youth Mental Health, Parkville, VIC, Australia; Department of Psychiatry, University of Melbourne, Parkville, VIC, Australia. 7. Centre for Molecular and Medical Research, School of Medicine, Deakin University, Geelong, VIC, Australia; Deakin University, IMPACT, the Institute for Mental and Physical Health and Clinical Translation, Barwon Health, Geelong, VIC, Australia.
Abstract
BACKGROUND: Elevated levels of systemic inflammation are consistently reported in both schizophrenia (SZ) and bipolar-I disorder (BD), and are associated with childhood trauma exposure. We tested whether childhood trauma exposure moderates associations between systemic inflammation and brain morphology in people with these diagnoses. METHODS: Participants were 55 SZ cases, 52 BD cases and 59 healthy controls (HC) who underwent magnetic resonance imaging. Systemic inflammation was measured using a composite z-score derived from serum concentrations of interleukin 6, tumor necrosis factor alpha and C-reactive protein. Indices of grey matter volume covariation (GMC) were derived from independent component analysis. Childhood trauma was measured using the Childhood Trauma Questionnaire (CTQ Total score). RESULTS: A series of moderated moderation analyses indicated that increased systemic inflammation were associated with increased GMC in the striatum and cerebellum among all participants. Severity of childhood trauma exposure moderated the relationship between systemic inflammation and GMC in one component, differently among the groups. Specifically, decreased GMC in the PCC/precuneus, parietal lobule and postcentral gyrus, and increased GMC in the left middle temporal gyrus was associated with increased systemic inflammation in HC individuals exposed to high (but not low or average) levels of trauma and in SZ cases exposed to low (but not average or high) levels of trauma, but not in BD cases. CONCLUSIONS: Increased systemic inflammation is associated with grey matter changes in people with psychosis, and these relationships may be partially and differentially moderated by childhood trauma exposure according to diagnosis.
BACKGROUND: Elevated levels of systemic inflammation are consistently reported in both schizophrenia (SZ) and bipolar-I disorder (BD), and are associated with childhood trauma exposure. We tested whether childhood trauma exposure moderates associations between systemic inflammation and brain morphology in people with these diagnoses. METHODS: Participants were 55 SZ cases, 52 BD cases and 59 healthy controls (HC) who underwent magnetic resonance imaging. Systemic inflammation was measured using a composite z-score derived from serum concentrations of interleukin 6, tumor necrosis factor alpha and C-reactive protein. Indices of grey matter volume covariation (GMC) were derived from independent component analysis. Childhood trauma was measured using the Childhood Trauma Questionnaire (CTQ Total score). RESULTS: A series of moderated moderation analyses indicated that increased systemic inflammation were associated with increased GMC in the striatum and cerebellum among all participants. Severity of childhood trauma exposure moderated the relationship between systemic inflammation and GMC in one component, differently among the groups. Specifically, decreased GMC in the PCC/precuneus, parietal lobule and postcentral gyrus, and increased GMC in the left middle temporal gyrus was associated with increased systemic inflammation in HC individuals exposed to high (but not low or average) levels of trauma and in SZ cases exposed to low (but not average or high) levels of trauma, but not in BD cases. CONCLUSIONS: Increased systemic inflammation is associated with grey matter changes in people with psychosis, and these relationships may be partially and differentially moderated by childhood trauma exposure according to diagnosis.
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