Brain morphology links systemic inflammation to cognitive function in midlife adults |
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| Institution: | 1. Department of Medicine, Cedars Sinai Medical Center, Los Angeles, CA, United States;2. Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific and Graduate College of Biomedical Sciences, Western University of Health Sciences, Pomona, CA, United States;1. Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK;2. Department of Psychology, University of Edinburgh, UK;3. Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK;4. Edinburgh Delirium Research Group, Geriatric Medicine, University of Edinburgh, UK;5. Scottish Imaging Network, A Platform for Scientific Excellence (SINAPSE) Collaboration, Edinburgh, UK;1. Centre for Human Psychopharmacology, Swinburne University, Melbourne, Australia;2. Professorial Unit, The Melbourne Clinic, Department of Psychiatry, The University of Melbourne, Melbourne, Australia;3. Wesnes Cognition Ltd, Little Paddock, Streatley Hill, Streatley on Thames, RG8 9RD, UK;1. Institut National de la Santé et de la Recherche Médicale, U1061 Neuropsychiatrie, Montpellier, France;2. Faculty of Medicine, University of Montpellier, Montpellier, France;3. Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, Scotland, UK;4. Department of Psychiatry, School of Clinical Medicine, Cambridge Biomedical Campus, University of Cambridge, Cambridge, UK;5. Department of Psychiatry, University of Oxford, Oxford, UK;6. The Centre for Mental Health, Imperial College, London, UK;1. Institute for Policy Research, Northwestern University, Evanston, Illinois;2. Department of Psychology, Northwestern University, Evanston, Illinois;5. Department of Radiology, Northwestern Feinberg School of Medicine, Chicago, Illinois;6. Department of Psychiatry, Northwestern Feinberg School of Medicine, Chicago, Illinois;3. Center for Family Research, University of Georgia, Athens Georgia;4. Department of Psychology, University of Georgia, Athens Georgia;1. Massachusetts General Hospital, Department of Psychiatry, USA;2. Harvard Medical School, Department of Psychiatry, USA;3. University of Illinois at Chicago, Department of Psychiatry, USA;4. University of Utah, Department of Psychiatry, USA;5. Sunnybrook Health Sciences Centre, Department of Psychiatry, Canada;6. University of Toronto, Department of Pharmacology and Toxicology & Department of Psychiatry, Canada;7. Keck School of Medicine of the University of Southern California, Department of Pediatrics, USA |
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| Abstract: | Background: Inflammation is linked to cognitive decline in midlife, but the neural basis for this link is unclear. One possibility is that inflammation associates with adverse changes in brain morphology, which accelerates cognitive aging and later dementia risk. Clear evidence is lacking, however, regarding whether inflammation relates to cognition in midlife via changes in brain morphology. Accordingly, the current study examines whether associations of inflammation with cognitive function are mediated by variation in cortical gray matter volume among midlife adults. Methods: Plasma levels of interleukin (IL)-6 and C-reactive protein (CRP), relatively stable markers of peripheral systemic inflammation, were assessed in 408 community volunteers aged 30–54 years. All participants underwent structural neuroimaging to assess global and regional brain morphology and completed neuropsychological tests sensitive to early changes in cognitive function. Measurements of brain morphology (regional tissue volumes and cortical thickness and surface area) were derived using Freesurfer. Results: Higher peripheral inflammation was associated with poorer spatial reasoning, short term memory, verbal proficiency, learning and memory, and executive function, as well as lower cortical gray and white matter volumes, hippocampal volume and cortical surface area. Mediation models with age, sex and intracranial volume as covariates showed cortical gray matter volume to partially mediate the association of inflammation with cognitive performance. Exploratory analyses of body mass suggested that adiposity may be a source of the inflammation linking brain morphology to cognition. Conclusions: Inflammation and adiposity might relate to cognitive decline via influences on brain morphology. |
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| Keywords: | Inflammation Interleukin-6 C-reactive protein Gray matter volume Cognitive decline Brain atrophy Cognitive aging |
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