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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 609019, 8 pages
Research Article

Mild Systemic Oxidative Stress in the Subclinical Stage of Alzheimer’s Disease

1Instituto de Química, USP, Cidade Universitária, Avenida Lineu Prestes 748, 05508-900 São Paulo, SP, Brazil
2Instituto de Ciências Ambientais, Química e Farmacêuticas, UNIFESP, Rua Arthur Riedel 275, 09972-270 Diadema, SP, Brazil
3Departamento de Hematologia e Oncologia, FMABC, Avenida Príncipe de Gales 821, 09060-650 Santo André, SP, Brazil
4Departamento de Medicina, UNIFESP, Rua Sena Madureira 1500, 04021-001 São Paulo, SP, Brazil
5Departamento de Medicina Preventiva, UNIFESP, Rua Sena Madureira 1500, 04021-001 São Paulo, SP, Brazil

Received 14 July 2013; Accepted 8 November 2013

Academic Editor: Sara Mostafalou

Copyright © 2013 Leandro Giavarotti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Alzheimer’s disease (AD) is a late-onset, progressive degenerative disorder that affects mainly the judgment, emotional stability, and memory domains. AD is the outcome of a complex interaction among several factors which are not fully understood yet; nevertheless, it is clear that oxidative stress and inflammatory pathways are among these factors. 65 elderly subjects (42 cognitively intact and 23 with probable Alzheimer’s disease) were selected for this study. We evaluated erythrocyte activities of superoxide dismutase, catalase, and glutathione peroxidase as well as plasma levels of total glutathione, α-tocopherol, β-carotene, lycopene, and coenzyme Q10. These antioxidant parameters were confronted with plasmatic levels of protein and lipid oxidation products. Additionally, we measured basal expression of monocyte HLA-DR and CD-11b, as well as monocyte production of cytokines IL1-α, IL-6, and TNF-α. AD patients presented lower plasmatic levels of α-tocopherol when compared to control ones and also higher basal monocyte HLA-DR expression associated with higher IL-1α production when stimulated by LPS. These findings support the inflammatory theory of AD and point out that this disease is associated with a higher basal activation of circulating monocytes that may be a result of α-tocopherol stock depletion.