Increased low-density lipoprotein oxidation,but not total plasma protein oxidation,in Alzheimer's disease |
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Authors: | Sarah Aldred Stuart Bennett Patrizia Mecocci |
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Institution: | 1. Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA;2. Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA;1. The James Buchanan Brady Urological Institute and Department of Urology, The Johns Hopkins School of Medicine, Baltimore, MD;2. Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC;1. Global Formulation Research-US, Eisai Inc., 900 Davis Drive, RTP, NC 27709, USA;2. Analytical Research Laboratory, Eisai Co., Ltd., 1-3, Tokodai 5-Chome, Tsukuba, Ibaraki 300-2635, Japan |
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Abstract: | ObjectivesThe two most common forms of dementia are Alzheimer's disease (AD), and vascular dementia (VaD). In the overlap of biochemical processes which have been identified in AD and VaD, oxidative stress is believed to contribute to the numerous pathologies of both dementias.Design and methodsThis study assessed oxidative damage in total plasma proteins, and isolated LDL in AD patients and age matched controls, in addition total antioxidant capacity (TAC) was measured.ResultsSignificantly higher LDL protein carbonylation was observed in AD compared to age-matched controls (AD: 4.17 ± 0.73 vs. control: 3.85 ± 0.86 nmol/mg LDL; p = 0.05, 2-tailed Mann–Whitney), in addition to reduced TAC (AD: 924.708 ± 174.429 vs. control: 1078.536 ± 252.633 μM; p = 0.001, 2-tailed Mann–Whitney). No differences were seen in total plasma protein carbonyl content (AD: 3.88 ± 0.31 vs. control: 3.98 ± 0.48 nmol/mg protein).ConclusionThe results further support the view that oxidation events in AD may be specific in nature, and represent functional changes to proteins, rather than random global events. |
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