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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences Advance Access published online on June 16, 2009
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, doi:10.1093/gerona/glp074
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© The Author 2009. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Nitric Oxide Activity and Isoenzyme Expression in the Senescence-Accelerated Mouse P8 Model of Alzheimer’s Disease: Effects of Anti-Amyloid Antibody and Antisense Treatments

Abbas K. Ali, William A. Banks, Vijaya B. Kumar, Gul N. Shah, Jessica L. Lynch, Susan A. Farr, Melissa A. Fleegal-DeMotta and John E. Morley

Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center–St Louis, Missouri, and Department of Internal Medicine, Division of Geriatrics, Saint Louis University School of Medicine, Missouri

Address correspondence to William A. Banks, MD, Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center–St Louis, 915 North Grand Boulevard, St Louis, MO 63106. Email: bankswa{at}slu.edu


  Abstract

Amyloid beta protein (Aβ) in Alzheimer’s disease induces oxidative stress through several mechanisms, including stimulation of nitric oxide synthase (NOS) activity. We examined NOS activity and expression in the senescence-accelerated mouse P8 (SAMP8) line. The SAMP8 strain develops with aging cognitive impairments, increases in Aβ, and oxidative stress, all reversed by amyloid precursor protein antisense or Aβ antibody treatment. We found here that hippocampal NOS activity in 12-month-old SAMP8 mice was nearly double that of 2-month-old SAMP8 or CD-1 mice, but with no change in NOS isoenzyme mRNA and protein levels. Antisense or antibody treatment further increased NOS activity in aged SAMP8 mice. Antisense treatment increased inducible NOS (iNOS) mRNA levels, decreased neuronal NOS mRNA and protein levels, but did not affect endothelial NOS (eNOS) or iNOS protein or eNOS mRNA levels. These results suggest a complex relation between Aβ and NOS in the SAMP8 that is largely mediated through posttranslational mechanisms.

Keywords Alzheimer's disease; Nitric oxide synthase; Nitric oxide; Amyloid beta protein; SAMP8; antisense; mRNA; antibody

Received: August 12, 2008; Accepted: May 14, 2009

Decision Editor: Huber R. Warner, PhD


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