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Article type: Research Article
Authors: Montine, Thomas J.; * | Quinn, Joseph F. | Montine, Kathleen S. | Kaye, Jeffrey A. | Breitner, John C.S.
Affiliations: Departments of Pathology and Psychiatry, University of Washington, Seattle, WA, Department of Neurology, Oregon Health & Science University, and Veteran's Administration Medical Centers in Portland, OR, and Seattle, WA, USA
Correspondence: [*] Corresponding author: Thomas J. Montine, MD, PhD, University of Washington, Department of Pathology, Harborview Medical Center, Box 359791, 300 9th Ave, Seattle, WA 98104, USA. Tel.: +1 206 731 6776; Fax: +1 206 341 5249; E-mail: tmontine@u.washington.edu.
Abstract: Dementia from Alzheimer's disease (AD) represents a significant and growing public health burden and presents a clear therapeutic imperative. Key to success in this undertaking will be biomarkers for the objective assessment of disease progression and response to therapeutics. Oxidative damage is one facet of AD pathogenesis for which there are experimentally validated quantitative in vivo biomarkers, the F2-isoprostanes (IsoPs). While plasma- or urine-based assays are desirable, consistent and reproducible cross-sectional data for increased F2-IsoPs in AD and mild cognitive impairment have been obtained only for CSF. In addition, measurement of CSF F2-IsoPs can increase the accuracy of laboratory-based classification of geriatric dementias, and have been used to assess objectively the response to anti-oxidant interventions in AD.
Keywords: Alzheimer's disease, biomarkers, F2-isoprostanes, oxidative stress
DOI: 10.3233/JAD-2005-8405
Journal: Journal of Alzheimer's Disease, vol. 8, no. 4, pp. 359-367, 2005
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