Abstract
Background: Increasing evidence suggests that oxidative stress is associated with normal aging and several neurodegenerative diseases, including Alzheimer’s disease. Alzheimer’s disease is a progressive neurodegenerative disorder whose clinical manifestations appear in old age. Lipid peroxidation plays an important role in the development of dementia and AD. Elevated plasma homocysteine has been associated with pathogenesis of AD. The aim of the present study was to determine relationship between Hcy level and AD and its relationship oxidative stress biomarkers. Thirty AD patients and thirty healthy controls participated in the study. Plasma total Hcy and serum Malondialdehyde, activity of RBC-SOD, RBC-GSH (reduced Glutathione), serum Total thiol proteins and plasma Total Antioxidant Capacity were measured both in patients and controls using spectrophotometric methods. Competitive chemiluminescent immunoassay was used to analyse the total level of homocysteine in plasma. The lipid peroxidation in serum was measured by the level of TBARS. RBC-Superoxide dismutase activity and GSH were assayed by the method of Das and Burtis-Ashwood respectively. Serum thiol proteins (-SH) was determined by Habeeb method. TAC in plasma was analyzed by FRAP assay. Results: The plasma levels of Hcy and serum MDA in AD group are significantly higher than that of normal controls. The activity of RBC-SOD in AD group is significantly lower than that of normal control group. The significant decrease in the levels of RBC-GSH, total thiol proteins and TAC was observed in AD patients compared to controls. Furthermore, there were significant positive correlations between the plasma Hcy and MDA levels (r = +0.42, p= 0.01) and significant negative correlations between the levels plasma Hcy and TAC (r = -0.40, p= 0.02) in AD group. Conclusion: Hcy participate in pathogenesis of AD and elevated Hcy can promote significant oxidant damage and enhance oxidative stress in AD. This may represent additional risk factor pathways which conspire to produce AD. Increased oxidative stress and decreased antioxidants indicated its association with AD progression.
