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Mild Systemic Oxidative Stress in the Subclinical Stage of Alzheimer’s Disease
Author(s) -
Leandro Giavarotti,
Karin Simon,
Lígia Ajaime Azzalis,
Fernando Luiz Affonso Fonseca,
Alessandra F. Lima,
Maria C. V. Freitas,
Milena Karina Coló Brunialti,
Reinaldo Salomão,
Alcione A. V. S. Moscardi,
Maria Beatriz Marcondes Macedo Montaño,
Luiz Roberto Ramos,
Virgínia Junqueira
Publication year - 2013
Publication title -
oxidative medicine and cellular longevity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.494
H-Index - 93
eISSN - 1942-0900
pISSN - 1942-0994
DOI - 10.1155/2013/609019
Subject(s) - oxidative stress , superoxide dismutase , glutathione peroxidase , medicine , endocrinology , coenzyme q10 , alzheimer's disease , antioxidant , monocyte , immunology , chemistry , disease , biochemistry
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-1 α 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.

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