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

The etiopathogenesis of alzheimer’s disease (ad) is still unclear. however, long-termoxidative stress is believed to be one of the major contributing factors in progression of neuronaldegeneration and decline of cognitive function in ad. in order to assess the presence of oxidative stressin ad, we examined the enzymatic activities of the erythrocyte cu-zn superoxide dismutase (cu-znsod), 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 sodactivity was significantly higher and the level of gsh-px and tas activities were significantly lower inad 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 activitywas 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 inthe pathogenesis underlying ad neurodegeneration. in addition, the enzymatic activity of theerythrocyte cu-zn sod and gsh-px and the plasma level of tas can be used as a measure of theoxidative stress and a marker for pathological changes in the brain of patients with ad.