Table 2.

Major effects of oxidative stress in the pathogenesis of Alzheimer's disease.

Effects of ROS	Result	Biological evidence(s)
Protein oxidation	Increased protein carbonyl content	Increased protein oxidation in frontal pole and occipital pole [113] Decreased ratio of (MAL-6)/(W/S) in AD hippocampus and inferior parietal lobule, decreased the W/S ratio in in vitro models of human synaptosomes oxidation by ROS [114]
DNA oxidation	Direct damage to DNA structure	3-fold increase in mitochondrial DNA oxidation in parietal cortex in AD [115] Increase in oxidative damage to nuclear DNA in AD compared with age-matched control subjects [116] 8-hydroxy-2-deoxyguanosine as a marker of DNA oxidation increases in AD [117]
Lipid peroxidation	Brain phospholipid damage	Increased TBARS levels in AD in hippocampus, piriform cortex, and amygdala [118] Increased lipid peroxidation of AD brain homogenates in vitro due to Fe-H2O2 [119] Increased apoptosis in cultured DS and AD neurons inhibited by antioxidant enzymes [112, 120] Decrease in PC, PE, phospholipid precursors, choline, and ethanolamine in hippocampus and inferior parietal lobule in AD [121] Increased aldehydes as a cytotoxic agent in the brain of AD patients [122]
Antioxidant enzymes	Changes in enzymes contents	Elevated GSH-Px, GSSG-R, and CAT activity in hippocampus and amygdala in AD [118] Many studies showed no elevation in enzyme activity [123, 124] or decrease in activity [125]
AGE formation	Pathological changes in protein structure and action	Accelerates aggregation of soluble nonfibrillar Aβ and tau [126]

MAL-6: weakly immobilized protein bound spin label; W/S: strongly immobilized protein bound spin label; TBARS: thiobarbituric acid reactive substances; DS: Down syndrome; PC: phosphatidylcholine; PE: phosphatidylethanolamine; GSH-Px: glutathione peroxidase; GSSG-R: glutathione reductase; CAT: catalase; AGE: advanced glycation end products.