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Abstract
Several lines of evidence support the hypothesis that oxygen free radicals are involved in the destruction of neurons in various degenerative disorders of the central nervous system. The activities of superoxide dismutase, catalase and glutathione peroxidase, three enzymes that contribute to the cellular defenses against free radical damage, were measured in different areas of autopsy brains from patients with Alzheimer's disease and from age matched controls. All brains were removed within 24 hours of the time of death and were cut in half sagitally. One half was stored frozen at -86° C and the other half was examined histologically to confirm the presence or absence of Alzheimer's disease. Samples were taken from the frozen half for the enzyme assays.
In control brains, the activity of superoxide dismutase is significantly higher in the cerebellum, frontal cortex and hippocampus than it is in the temporal cortex, parietal cortex and entorhinal cortex. The activity of catalase is significantly higher in cerebellum and frontal cortex than in hippocampus, parietal cortex and entorhinal cortex. Glutathione peroxidase activity is uniform across all brain areas studied.
In Alzheimer's brains, superoxide dismutase activity is not statistically different among the various brain regions studied, but it is significantly lower than control in the cerebellum (–27%), frontal cortex (-27%) and hippocampus (-35%). Catalase is significantly higher in Alzheimer's cerebellum, frontal cortex and temporal cortex than in Alzheimer's hippocampus, parietal cortex and entorhinal cortex. However, there are no significant differences in catalase activity between Alzheimer's and control samples. Glutathione peroxidase activity is the same in all areas of control and Alzheimer's brains studied and does not differ between control and Alzheimer's samples.
The lower superoxide dismutase activity in certain Alzheimer's brain regions indicates impaired free radical defenses and is consistent with an increased vulnerability of these brain areas to oxidative damage.
