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Acceleration of phosphatidylcholine synthesis and breakdown by inhibitors of mitochondrial function in neuronal cells: a model of the membrane defect of Alzheimer’s disease

STEVEN A. FARBER^*, BARBARA E. SLACK and JAN KRZYSZTOF BLUSZTAJN¹

^* Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA; and
Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, USA

¹Correspondence: Boston University School of Medicine, 85 East Newton St., Room M1009, Boston, MA 02118, USA. E-mail: jbluszta{at}bu.edu

Brain cells in Alzheimer’s disease (AD) exhibit a membrane defect characterized by accelerated phospholipid turnover. The mechanism responsible for this defect remains unknown. Recent studies indicate that impairment of mitochondrial function is frequently observed in AD and may be responsible for certain aspects of its pathophysiology. We show that when PC12 cells are exposed to inhibitors of mitochondrial bioenergetics, the turnover of their major membrane phospholipid, phosphatidylcholine, is accelerated, producing a pattern of metabolic changes that mimics that observed in brains of AD patients. Abnormalities of mitochondrial function may therefore underlie the membrane defect in AD.—Farber, S. A., Slack, B. E., Blusztajn, J. K. Acceleration of phosphatidylcholine synthesis and breakdown by inhibitors of mitochondrial function in neuronal cells: a model of the membrane defect of Alzheimer’s disease.

Key Words: PC 12 cells • membrane turnover • phospholipase • CTP:phosphorylcholine cytidylyltransferase • glycerophosphorylcholine

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