The Effects of Different Antioxidants on the Activity of Cerebrocortical MnSOD and Na,K-ATPase from post mortem Alzheimer’s Disease and Age-matched Normal Brains

ISSN: 1875-5828 (Online)
ISSN: 1567-2050 (Print)


Volume 11, 10 Issues, 2014


Download PDF Flyer




Current Alzheimer Research

Aims & ScopeAbstracted/Indexed in

Ranking and Category:
  • 35th of 193 in Clinical Neurology
  • 80th of 252 in Neurosciences

Submit Abstracts Online Submit Manuscripts Online

Editor-in-Chief:
Prof. Debomoy K. Lahiri
Department of Psychiatry Indiana University School of Medicine
Indianapolis, IN
USA


View Full Editorial Board

Subscribe Purchase Articles Order Reprints

Current: 3.676
5 - Year: 4.203

The Effects of Different Antioxidants on the Activity of Cerebrocortical MnSOD and Na,K-ATPase from post mortem Alzheimer’s Disease and Age-matched Normal Brains

Author(s): C. Kairane, R. Mahlapuu, K. Ehrlich, M. Zilmer and U. Soomets

Affiliation: Department of Biochemistry, Faculty of Medicine, University of Tartu, The Centre of Excellence of Translational Medicine, Ravila Str. 19, Tartu, 50411, Estonia.

Abstract

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.

Download Free Rights and Permissions

Article Details

Volume: 11
Issue Number: 1
First Page: 79
Last Page: 85
Page Count: 7
DOI: 10.2174/15672050113106660179
Advertisement

Related Journals




Webmaster Contact: urooj@benthamscience.org Copyright © 2014 Bentham Science