Research Article Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress W. Swardfager, 1,2,3,4,5 N. Herrmann, 1,2,3,6 A. C. Andreazza, 6 R. H. Swartz, 4 M. M. Khan, 1 S. E. Black, 3,4,5 and K. L. Lanctôt 1,2,3,6 1 Neuropsychopharmacology Research Group, Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5 2 Department of Psychiatry, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5 3 Canadian Partnership for Stroke Recovery, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5 4 Division of Cognitive Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, Toronto, ON, Canada M4N 3M5 5 L.C. Campbell Cognitive Neurology Research Unit, Sunnybrook Research Institute, Toronto, ON, Canada M4N 3M5 6 Department of Psychiatry, University of Toronto, 250 College Street, 8th Floor, Toronto, ON, Canada M5T 1R8 Correspondence should be addressed to K. L. Lanctˆ ot; krista.lanctot@sunnybrook.ca Received 8 April 2014; Revised 13 May 2014; Accepted 27 May 2014; Published 18 June 2014 Academic Editor: Eng-King Tan Copyright © 2014 W. Swardfager et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinfammatory cytokines (IL-17, IL-23, and interferon- [IFN-] ), anti-infammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status ( 1,46 = 8.44,  = 0.006). IL-17 concentrations did not difer between subjects with and without depressive symptoms ( 1,46 = 8.44,  = 0.572); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms ( 1,46 = 9.29,  = 0.004). In those subjects with depressive symptoms, IL-17 was associated with higher LPH ( = 0.518,  = 0.023) and lower IL-10 ( = −0.484,  = 0.036), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinfammatory and anti-infammatory activity and increased oxidative stress. 1. Introduction Stroke is a leading cause of disability, and common sequelae such as depression and cognitive impairment contribute signifcantly to disease burden among survivors. Depression afer stroke has been associated with cognitive impairment, as assessed using the Mini Mental State Examination (MMSE) [1, 2]; however, biological mechanisms that may mediate this relationship remain elusive. Depression in medically healthy patients has been associated with increased concentrations of cytokines in peripheral blood [3], which may be relevant to depression afer stroke [4]. Previous studies have identifed relationships between MMSE scores and peripheral blood infammatory markers, including C-reactive protein and kynurenine [5, 6], suggesting infammation as a possible link between depression and cognitive impairment afer stroke. In animal models, the infltration of T cells that express IL-17 exacerbates neurodegenerative damage in the delayed phase of postischemic injury [7]. In the peri-infarct cortex, apoptosis is the predominant mode of neuronal death, which is heavily infuenced by infammatory and anti-infammatory cytokine signals released from infltrating peripheral T lym- phocytes and other cell types; however, only a few clinical studies have investigated IL-17 afer stroke [8, 9]. In one study, IL-17 expression by peripheral mononuclear cells was associated with poorer neurological outcomes, although relationships with depression and cognitive status were not assessed [10]. IL-17 can induce blood brain barrier disruption Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 245210, 6 pages http://dx.doi.org/10.1155/2014/245210