Research article summary (published 3 Aug 2009):

Oxygen treatment triggers cognitive impairment in Alzheimer's transgenic mice.

Full Abstract

An association between major surgery in the elderly and precipitation of Alzheimer's disease has been reported. As 100% oxygen (hyperoxia) is commonly administered after surgery, we exposed cognitively unimpaired Alzheimer's transgenic mice to hyperoxia typical of human exposure in a hospital setting. Three-hour hyperoxia treatments to young adult Alzheimer's transgenic mice: (i) triggered cognitive impairment that was not otherwise present at that age, (ii) increased aberrant brain synaptophysin staining, and (iii) increased brain levels of isofurans (products of lipid peroxidation sensitive to hyperoxia). Thus, hyperoxia-induced synaptic dysfunction and brain oxidative stress are likely the triggering mechanisms of cognitive dysfunction in Alzheimer's mice. These results may suggest that exposure of elderly patients to excessive amounts of oxygen perioperatively hastens the development of Alzheimer's disease.

Author information

Author/s: Arendash, Gary W (GW); Cox, April A (AA); Mori, Takashi (T); Cracchiolo, Jennifer R (JR); Hensley, Kenneth L (KL); Roberts, L Jackson (LJ);

Affiliation: Florida Alzheimer's Disease Research Center, University of South Florida, Tampa, Florida 33620, USA. arendash(-atsign-)cas.usf.edu

Grants: AG025711 (Agency:NIA NIH HHS) ; GM42056 (Agency:NIGMS NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural

Journal: Neuroreport (Neuroreport), published in England. (Language: eng)

Reference: 2009-Aug; vol 20 (issue 12) : pp 1087-92

Dates: Created 2009/07/10; Completed 2009/09/29;

PMID: 19543132, status: MEDLINE (last retrieval date: 9/29/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Alzheimer Disease - complications; metabolism Amyloid beta-Protein Precursor - genetics Animals Brain - metabolism Cognition Disorders - etiology; metabolism Disease Models, Animal Humans Learning Disorders - etiology; metabolism Lipid Peroxidation Maze Learning - physiology

Maze Learning - physiology Memory Disorders - etiology; metabolism Memory, Short-Term - physiology Mice Mice, Transgenic Oxygen - toxicity Receptors, Cell Surface - genetics Reversal Learning - physiology Swimming Synaptophysin - metabolism

Associated Chemicals: Amyloid beta-Protein Precursor (0) ; Receptors, Cell Surface (0) ; Synaptophysin (0) ; protease nexins (0) ; Oxygen (7782-44-7)

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