THE STUDY OF ASSOCIATION OF OXIDATIVE STRESS AND INFLAMMATORY MARKERS AND IMPACT OF ANTIOXIDANTS SUPPLEMENTATION IN ALZHEIMER’S DISEASE

Alzheimer’s disease [AD] is an age-related progressive neurodegenerative disease caused by severe neurodegeneratioin in the hippocampus and neocortical regions of the brain of affected individuals. There is growing evidences also suggests increased oxidative stress and inflammation in patients with AD. Here, we assessed association of oxidative stress and inflammation in patients with AD. For this, we determined Malondialdehyde [MDA], Nitric oxide [NO] metabolites, Erythrocyte-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 on these parameters in AD patients. The correlation between ADA with parameters of oxidative stress was also evaluated. Statistical analysis was performed using student’t’ test. Serum MDA [p<0.0001], NO metabolites and ADA [p<0.0001] levels were found to be significantly high in patients when compared to controls. Significant decreased levels of RBC-GSH and TAC [p<0.0001] level in 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 that increased serum ADA activity indicates inflammation and increased MDA with decreased antioxidant capacity indicates oxidative stress in AD patients. Increased inflammatory and oxidative stress biomarkers and there correlation indicating their association and that are tightly linked to and neuronal loss and other pathophysiological processes in patients with AD. The data showed that decrease in MDA and ADA levels and increase in TAC after antioxidant supplementation. These results are more significant than that obtained by only regular treatment group. Thus, antioxidants trials are beneficial to prevent or reduce the progression of disease by minimizing oxidative damage and to certain limits modulate inflammatory consequences causes neuronal loss in AD.