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Departments of Neurology (Dr. Parker and J. Parks), Pediatrics (Dr. Parker), and Pathology (Dr. Kleinschmidt-DeMasters), University of Colorado School of Medicine, and the Veterans Administration Hospital (Dr. Filley), Denver, CO.
Previous work suggested a deficiency in the terminal complex of the mitochondrial electron transport chain, cytochrome c oxidase (COX), in platelet mitochondria of Alzheimer's disease (AD) patients. The present study extends this observation to AD brain mitochondria through assay of electron transport chain activities in mitochondria isolated from autopsied brain samples from AD patients (n = 9) and from controls with and without known neurologic disease (n = 8). AD brain mitochondria demonstrated a generalized depression of activity of all electron transport chain complexes. This depression was most marked in COX activity (p < 0.001). Concentrations of cytochromes b, c1 and aa3 were similar in AD and controls. The electron transport chain is defective in AD brain, and the defect centers about COX.
Address correspondence and reprint requests to Dr. W. D. Parker, Department of Neurology, University of Virginia Medical Center, Charlottesville, VA 22908.
Supported by NIH grants NS25382 and AGO9417 and by a grant from the American Parkinson's Disease Association.
Presented in part at the Second International Conference on Human Mitochondria1 Pathology, Rome, 1992.
Received August 13, 1993. Accepted for publication in final form November 24,1993.
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