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From the Departments of Neurology (Drs. Tamaoka, Miyatake, Matsuno, Ishii, and Shoji) and Nephrology (Dr. Nagase), Institute of Clinical Medicine, University of Tsukuba; the Department of Neuroscience (Drs. Sahara and Mori), Osaka City University Medical School; the Departments of Neurology (Dr. Tsuji) and Pathology (Drs. Takahashi and Wakabayashi), Brain Research Institute, Niigata University; and the Department of Neurology (Dr. Ono), Teikyo University School of Medicine Ichihara Hospital, Chiba, Japan.
Address correspondence and reprint requests to Dr. A. Tamaoka, Department of Neurology, Institute of Clinical Medicine, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki 305-0006, Japan.
Thiobarbituric acidreactive substances (TBARS), an index of lipid peroxidation, were assayed in postmortem brain. Basal TBARS levels were increased and oxidative stimulation produced more TBARS in AD relative to control brains. In addition, apolipoprotein E isoforms showed differing antioxidant activities, with E2 > E3 > E4, suggesting that the lowest antioxidant activity of E4 could contribute to its association with AD.
Key words: ADAPOELipid peroxidationThiobarbituric acidreactive substancesOxidative stress.
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