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Enhanced brain levels of 8,12-iso-iPF₂-VI differentiate AD from frontotemporal dementia

From The Center for Experimental Therapeutics, Department of Pharmacology (Y. Yao, S. Sung, and Dr. Praticò), Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine (Drs. Lee, Trojanowski, and Zhukareva), and Department of Neurology (Dr. Clark), University of Pennsylvania, School of Medicine, Philadelphia; and Department of Chemistry (Dr. Rokach), Florida Institute of Technology, Melbourne.

Address correspondence and reprint requests to Dr. Domenico Praticò, Center for Experimental Therapeutics, 812, BRB 2/3, 421 Curie Blvd, Philadelphia, PA 19104; e-mail: domenico{at}spirit.gcrc.upenn.edu

Objective: To quantify the isoprostane 8,12-iso-iPF₂-VI in brain tissues obtained from patients with AD, patients with frontotemporal dementia (FTD), and controls.

Background: Enhanced brain oxidative stress with secondary damage to cellular macromolecules may play a role in the pathogenesis of AD and FTD. The isoprostane 8,12-iso-iPF₂-VI is a specific and sensitive marker of in vivo lipid peroxidation and is increased in AD.

Methods: Levels of this isoprostane were determined by gas chromatography/negative ion chemical ionization mass spectrometry.

Results: Levels of 8,12-iso-iPF₂-VI were markedly elevated in both frontal and temporal cortex of AD brains compared to the corresponding areas of FTD and controls. No significant difference in brain 8,12-iso-iPF₂-VI levels for any regions considered was observed between FTD and controls.

Conclusions: Lipid peroxidation is a feature of AD, but not FTD. The generation of 8,12-iso-iPF₂-VI in the brain is not a general or final common pathway of neurodegeneration, but may be relatively specific for disease processes in AD and not FTD.

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