Association of Inflammatory Consequences with Oxidative Stress and the Impact of Antioxidants Supplementation in Alzheimer’s Disease

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Alzheimer's disease [AD] is an age-related progressive neurodegenerative disease characterized by severe neurodegeneration in affected individuals' hippocampus and neocortical regions of the brain. Inflammation and oxidative stress can contribute to the development and progression AD. Here, we assessed the association of oxidative stress with inflammation in the pathophysiological consequences in patients with AD. For this, we determined Malondialdehyde [MDA], Nitric oxide [NO] metabolites, Erythrocyte-GSH (RBC-GSH), total antioxidant capacity [TAC] and the activity of Adenosine deaminase [ADA] as inflammatory marker levels and compared with controls. We also aimed to estimate the influence of antioxidant supplementation in AD. The correlation between ADA with parameters of oxidative stress was also evaluated. Significant increase in the levels of oxidative and inflammatory parameters was observed in patients. Significant decreased levels of antioxidants were observed in patients with AD. The significant positive correlation was found between ADA and MDA levels and negative correlation between ADA activity and the levels RBC-GSH and TAC. We conclude from the observation that the increased serum ADA activity indicates inflammatory consequences and increased MDA with decreased antioxidant capacity indicates oxidative stress in AD patients. Increased inflammatory and oxidative stress biomarkers, as well as their correlation, are strongly linked to neuronal loss and other pathophysiological processes in Alzheimer's disease patients. The data showed that antioxidant supplementation reduced MDA and ADA levels while increasing TAC. These findings are more significant than those obtained by the regular treatment group alone. Thus, antioxidant trials would be beneficial in preventing or slowing disease progression by minimizing oxidative damage and, to a certain extent, modulating inflammatory consequences that prevent further neuronal loss in AD.