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Mediators of Inflammation
Volume 2013 (2013), Article ID 615745, 9 pages
Clinical Study

Elevated Osteopontin Levels in Mild Cognitive Impairment and Alzheimer’s Disease

1Department of Neurology, Bei Jing Daopei Hospital, Bei Jing 100749, China
2Department of Emergency, The Fourth Affiliated Hospital of Harbin Medical University, Harbin 150001, China
3Department of Paediatrics, Daqing Oilfied General Hospital, Daqing 163311, China
4Department of Neurology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China

Received 15 November 2012; Revised 30 January 2013; Accepted 14 February 2013

Academic Editor: Muzamil Ahmad

Copyright © 2013 Yuan Sun 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.


Inflammatory mediators are closely associated with the pathogenesis of neurodegenerative changes in Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Osteopontin (OPN) is a proinflammatory cytokine that has been shown to play an important role in various neuroinflammatory diseases. However, the function of OPN in AD and MCI progression is not well defined. Cerebrospinal fluid (CSF) and plasma samples were obtained from 35 AD patients, 31 MCI patients, and 20 other noninflammatory neurologic diseases (OND). Concentrations of OPN in the CSF and plasma were determined by enzyme-linked immunosorbent assay. During a 3-year clinical followup, 13 MCI patients converted to AD (MCI converters), and 18 were clinically stable (MCI nonconverters). CSF OPN concentrations were significantly increased in AD and MCI converters compared to OND, and increased levels of OPN in AD were associated with MMSE score; OPN protein levels both in the CSF and plasma of newly diagnosed AD patients were higher than that of chronical patients. In MCI converters individuals tested longitudinally, both plasma and CSF OPN concentrations were significantly elevated when they received a diagnosis of AD during followup. Further wide-scale studies are necessary to confirm these results and to shed light on the etiopathogenic role of osteopontin in AD.