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

• Autor(a) principal: Giavarotti, Leandro
• Data de Publicação: 2013
• Outros Autores: Simon, Karin A. [UNIFESP], Azzalis, Ligia A. [UNIFESP], Fonseca, Fernando L. A. [UNIFESP], Lima, Alessandra F. [UNIFESP], Freitas, Maria C. V. [UNIFESP], Brunialti, Milena K. C. [UNIFESP], Salomao, Reinaldo [UNIFESP], Moscardi, Alcione A. V. S. [UNIFESP], Montano, Maria B. M. M. [UNIFESP], Ramos, Luiz R. [UNIFESP], Junqueira, Virginia B. C. [UNIFESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNIFESP
• Texto Completo: http://repositorio.unifesp.br/handle/11600/35700; http://dx.doi.org/10.1155/2013/609019

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, alpha-tocopherol, beta-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-alpha, IL-6, and TNF-alpha. AD patients presented lower plasmatic levels of alpha-tocopherol when compared to control ones and also higher basal monocyte HLA-DR expression associated with higher IL-1 alpha 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 alpha-tocopherol stock depletion.