Among the markers and targets of the early phase of Alzheimer’s disease (AD) pathogenesis MnSOD (mitochondrial
dysfunction) and Na-pump (disturbances in function/regulation) are often highlighted. This paper focused on
comparison of the effects of three antioxidants on the activity of cerebrocortical MnSOD and Na,K-ATPase from post
mortem Alzheimer’s disease and age-matched normal brains. Antioxidant compounds with different origins: natural glutathione,
synthetic UPF peptides (glutathione analogues) and phytoestrogen genistein were investigated. Firstly, MnSOD
and Na,K-ATPase activities were found to be decreased in the post mortem AD brains compared with age-matched controls.
Secondly, GSH had no effect on MnSOD activity, but decreased Na,K-ATPase activity both in the control and AD
brains. Thirdly, UPF1 and UPF17 increased MnSOD activity, and UPF17 suppressed Na,K-ATPase activity. Further studies
are needed to clarify, if the inhibitory effect of UPF17 on Na,K-ATPase could abolish the beneficial effect gained from
MnSOD activation. Both the antioxidative potential of genistein and its potency to up-regulate Na,K-ATPase activity
make it an attractive candidate substance to suppress the early phase of the pathogenesis of AD.
Keywords: Alzheimer's disease, genistein, MnSOD, Na, K-ATPase, oxidative stress, UPF peptides.
Rights & PermissionsPrintExport