In the present study we observed a loss in excess of 1 3 of the copper transport and anti-oxidant protein ceruloplasmin in both the gray and white matter from superior temporal gyrus in Alzheimer's diseased brains compared to age-matched controls. A decrease in cerulopasmin could be reflected in decreased cellular metabolic processes such as the electron transport system and a decrease in the ability of the brain to protect itself from oxidative damage. Both decreased metabolic activity and an increase in oxidative insults are known to be associated with the neurological events in Alzheimer's disease, but the mechanism by which these phenomena occur are unknown. These results coupled with previous reports from this laboratory on iron regulatory proteins in the brain suggests one way in which cellular dysfunction and oxidative stress occurs in AD may be through a loss of ability to maintain a balance of essential metals.
All Science Journal Classification (ASJC) codes