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BioMed Research International
Volume 2014 (2014), Article ID 245210, 6 pages
Research Article

Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress

1Neuropsychopharmacology Research Group, Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5
2Department of Psychiatry, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5
3Canadian Partnership for Stroke Recovery, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Toronto, ON, Canada M4N 3M5
4Division of Cognitive Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, Toronto, ON, Canada M4N 3M5
5L.C. Campbell Cognitive Neurology Research Unit, Sunnybrook Research Institute, Toronto, ON, Canada M4N 3M5
6Department of Psychiatry, University of Toronto, 250 College Street, 8th Floor, Toronto, ON, Canada M5T 1R8

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. This 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). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-] γ), anti-inflammatory 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 ( , ). IL-17 concentrations did not differ between subjects with and without depressive symptoms ( , ); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms ( , ). In those subjects with depressive symptoms, IL-17 was associated with higher LPH ( , ) and lower IL-10 ( , ), 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 proinflammatory and anti-inflammatory activity and increased oxidative stress.