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Elevation of 12/15 lipoxygenase products in AD and mild cognitive impairment

Authors

  • Yuemang Yao BSc,

    1. Department of Pharmacology, University of Pennsylvania, School of Medicine, Philadelphia, PA
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  • Christopher M. Clark MD,

    1. Department of Neurology, University of Pennsylvania, School of Medicine, Philadelphia, PA
    2. Department of Alzheimer's Disease Center, University of Pennsylvania, School of Medicine, Philadelphia, PA
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  • John Q. Trojanowski MD, PhD,

    1. Department of Pathology and Laboratory Medicine, University of Pennsylvania, School of Medicine, Philadelphia, PA
    2. Center for Neurodegenerative Disease Research, University of Pennsylvania, School of Medicine, Philadelphia, PA
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  • Virginia M.-Y. Lee PhD,

    1. Department of Pathology and Laboratory Medicine, University of Pennsylvania, School of Medicine, Philadelphia, PA
    2. Center for Neurodegenerative Disease Research, University of Pennsylvania, School of Medicine, Philadelphia, PA
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  • Domenico Praticò MD

    Corresponding author
    1. Department of Pharmacology, University of Pennsylvania, School of Medicine, Philadelphia, PA
    • Department of Pharmacology, 3620 Hamilton Walk, John Morgan Building, Room 124, Philadelphia, PA 19104
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Abstract

The 12/15 lipoxygenase (12/15LOX) enzyme is increased in pathologically affected frontal and temporal regions of Alzheimer's disease (AD) brains compared with controls. Herein, we measured 12(S)-HETE and 15(S)-HETE levels, products of 12/15LOX, in cerebrospinal fluid (CSF) of normal individuals, subjects with mild cognitive impairment (MCI) and AD. Compared with controls, there was a significant increase of both metabolites in CSF from AD and MCI, which correlated with lipid peroxidation and tau protein levels. These results suggest that the activation of this enzyme occurs early in the course of AD, before the onset of overt dementia, thereby implicating 12/15LOX-mediated lipid peroxidation in the pathogenesis of AD. Ann Neurol 2005

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