Acceleration of phosphatidylcholine synthesis and breakdown by inhibitors of mitochondrial function in neuronal cells: a model of the membrane defect of Alzheimer's disease
| Autor: | S A, Farber, B E, Slack, J K, Blusztajn |
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| Rok vydání: | 2000 |
| Předmět: |
Neurons
Carbonyl Cyanide m-Chlorophenyl Hydrazone Cytidine Diphosphate Choline Membranes Time Factors Dose-Response Relationship Drug Uncoupling Agents Phosphorylcholine Glycerylphosphorylcholine PC12 Cells Choline Mitochondria Rats Disease Models Animal Alzheimer Disease Phosphatidylcholines Animals Enzyme Inhibitors Sodium Azide Dinitrophenols |
| Zdroj: | FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 14(14) |
| ISSN: | 0892-6638 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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