NEUROLOGY 1998;51:1014-1017
© 1998 American Academy of Neurology
Oxidative damage to DNA in lymphocytes from AD patients
P. Mecocci, MD, PhD,
M. C. Polidori, MD,
T. Ingegni, MD,
A. Cherubini, MD,
F. Chionne, MSc,
R. Cecchetti, BSc and
U. Senin, MD
From the Institute of Gerontology and Geriatrics (Drs. Mecocci, Polidori, Ingegni, Cherubini, and Senin, and R. Cecchetti), University of Perugia, and Service of Medical Physics (F. Chionne), Hospital of Perugia, Italy.
Address correspondence and reprint requests to Dr. Patrizia Mecocci, Institute of Gerontology and Geriatrics, University of Perugia, Via Eugubina, 42, 06122 Perugia, Italy.
Objective: Several studies show structural and functional alterations in peripheral cells in AD. The purpose of this study was to evaluate oxidative stress in AD lymphocytes.
Background: The literature supports the role of reactive oxygen species in the pathogenesis of AD because several markers of oxidative damage have been detected in AD brain.
Methods: 8-hydroxy-2'-deoxyguanosine (8OHdG), a marker of oxidative stress in DNA, was measured in lymphocytes of AD patients and healthy aged controls with high-pressure liquid chromatography with electrochemical detection, both at basal condition and after acute oxidative stress with hydrogen peroxide.
Results: A significantly higher concentration of 8OHdG in lymphocytes occurred in AD patients compared with controls. In this latter group, 8OHdG increased progressively with age. After acute oxidative stress, levels of formed 8OHdG did not differ between AD patients and controls.
Conclusions: Our results support that AD is affected by oxidative stress, detectable not only in the brain but also in peripheral cells; oxidative mechanisms may contribute to the pathogenesis of AD. Additional studies in other neurodegenerative diseases are needed to evaluate these findings.
Received January 29, 1998. Accepted in final form May 20, 1998.
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