Cortical Cytochrome Oxidase Activity Is Reduced in Alzheimer's Disease

Authors

  • Elizabeth M. Mutisya,

    1. Neurochemistry Laboratory, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.
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  • Allen C. Bowling,

    1. Neurochemistry Laboratory, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.
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  • M. Flint Beal

    Corresponding author
    1. Neurochemistry Laboratory, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.
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Address correspondence and reprint requests to Dr. M. F. Beal at Warren 408, Massachusetts General Hospital, Fruit St., Boston, MA 02114, U.S.A.

Abstract

Abstract: A defect in energy metabolism may play a role in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease. In the present study, we examined the activities of the enzymes that catalyze oxidative phosphorylation in frontal, temporal, parietal, and occipital cortex from Alzheimer's disease patients and age-matched controls. Complex I and complex II–III activities showed a small decrease in occipital cortex, but were unaffected in the other cortical areas. The most consistent change was a significant decrease of cytochrome oxidase (complex IV) activity of 25–30% in the four cortical regions examined. These results provide further evidence of a cytochrome oxidase defect in Alzheimer's disease postmortem brain tissue. A deficiency in this key energy-metabolizing enzyme could lead to a reduction in energy stores and thereby contribute to the neurodegenerative process.

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