ENZYMATIC an‎d NON-ENZYMATIC ANTIOXIDANT DEFENSE IN ALZHEIMER’S DISEASE

The etiopathogenesis of Alzheimer’s disease (AD) is still unclear. However, long-term oxidative stress is believed to be one of the major contributing factors in progression of neuronal degeneration and decline of cognitive function in AD. In order to assess the presence of oxidative stress in AD, we examined the enzymatic activities of the erythrocyte Cu-Zn superoxide dismutase (Cu-Zn SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and plasma level of total antioxidant status (TAS) in AD and control groups (age and sex-matched). The results showed that the Cu-Zn SOD activity was significantly higher and the level of GSH-Px and TAS activities were significantly lower in AD subjects compare to that in the control group (2111 ± 324 U/grHb, 43.7 ± 11.6 U/grHb, and 1.17 ± 0.23 mmol/l compared with 1371 ± 211 U/gr Hb; t = -2.17, P = 0.036, 56.3 ± 9.5 U/gr Hb; t = 3.8, P = 0.014, and 1.54 ± 0.2 mmol/l; t =11.18, P < 0.001, respectively). While, the erythrocyte CAT activity was lower in AD subjects compared to the control group, the difference was not statistically significant (t = 1.3, P = 0.15). These findings support the idea that the oxidative stress plays an important role in the pathogenesis underlying AD neurodegeneration. In addition, the enzymatic activity of the erythrocyte Cu-Zn SOD and GSH-Px and the plasma level of TAS can be used as a measure of the oxidative stress and a marker for pathological changes in the brain of patients with AD.