Journal
ANNALS OF NEUROLOGY
Volume 58, Issue 5, Pages 730-735Publisher
WILEY
DOI: 10.1002/ana.20629
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Funding
- NCI NIH HHS [CA68485, CA77839] Funding Source: Medline
- NCRR NIH HHS [RR00095] Funding Source: Medline
- NIA NIH HHS [5-P50-AG05144, 5-P01-AG05119] Funding Source: Medline
- NIDDK NIH HHS [DK48831] Funding Source: Medline
- NIGMS NIH HHS [GM15431] Funding Source: Medline
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Multiple studies demonstrate that the brain in Alzheimer's disease (AD) contains extensive oxidative damage. Most of these studies used advanced-stage AD patients raising the question of whether oxidative damage is a late effect of neurodegeneration or precedes and contributes to the pathogenesis of AD. Here we describe F-2-isoprostane (F-2-IsoP) and F-4-neuroprostane (F-4-NP) levels in longitudinally followed, well documented autopsied normal control subjects and patients with amnestic mild cognitive impairment (MCI), and late-stage AD. Gas chromatography/negative ion chemical ionization/mass spectrometry was used to determine F-2-IsoP and F-4-NP levels. Significant increases in F-2-IsoP levels were found in frontal, parietal and occipital lobes in MCI and late AD compared to controls but no significant differences were present between MCI and late AD. A significant increase in F-4-NPs was present in parietal and occipital lobes in MCI compared to controls and a significant increase was present in these regions and hippocampus in late AD compared to controls. The only difference betwen MCI and late AD was significantly increased F4-NP in hippocampus in late AD. Our data indicate that lipid peroxidation is present in the brain of MCI patients and suggest that oxidative damage may play a role in the pathogenesis of AD.
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