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Patrizia Mecocci, MD, PhD; M. Cristina Polidori, MD; Antonio Cherubini, MD, PhD; Tiziana Ingegni, MD; Paola Mattioli, MD; Marco Catani, MD; Patrizia Rinaldi, MD; Roberta Cecchetti, BSc; Wilhelm Stahl, PhD; Umberto Senin, MD; M. Flint Beal, MD

Arch Neurol. 2002;59:794-798.

Context  A large body of experimental evidence suggests that in Alzheimer disease (AD) pathogenesis an important role is played by oxidative stress, but there is still a lack of data on in vivo markers of free radical–induced damage.

Objectives  To evaluate levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative damage to DNA, in peripheral lymphocytes; to measure plasma concentrations of several nonenzymatic antioxidants; and to assess the relationships between any observed changes in lymphocyte DNA 8-OHdG content and plasma antioxidant levels in patients with AD and healthy aged control subjects.

Subjects  Forty elderly outpatients with AD and 39 healthy age- and sex-matched controls were studied.

Main Outcome Measures  The level of 8-OHdG was determined in DNA extracted from lymphocytes and plasma levels of vitamin C, vitamin A, vitamin E, and carotenoids (zeaxanthin, -cryptoxanthin, lycopene, lutein, and - and -carotene) were measured by high-performance liquid chromatography.

Results  Lymphocyte DNA 8-OHdG content was significantly higher and plasma levels of antioxidants (with the exception of lutein) were significantly lower in patients with AD compared with controls. In patients with AD, a significant inverse relationship between lymphocyte DNA 8-OHdG content and plasma levels of lycopene, lutein, -carotene, and -carotene, respectively, was observed.

Conclusions  Markers of oxidative damage are increased in AD and correlate with decreased levels of plasma antioxidants. These findings suggest that lymphocyte DNA 8-OHdG content in patients with AD reflects a condition of increased oxidative stress related to a poor antioxidant status.

From the Institute of Gerontology and Geriatrics, University of Perugia, Perugia, Italy (Drs Mecocci, Polidori, Cherubini, Ingegni, Mattioli, Catani, Rinaldi, Stahl, and Senin and Ms Cecchetti); Institute of Physiological Chemistry, Heinrich-Heine University, Düsseldorf, Germany (Drs Polidori and Stahl); and the Department of Neurology and Neuroscience, Weill Medical College of Cornell University and the New York Hospital, Cornell Medical Center, New York (Dr Beal).

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