Abnormal cholesterol processing in Alzheimer's disease patient's fibroblasts
Citation: Dufour F et al. Abnormal cholesterol processing in Alzheimer's disease patient's fibroblasts. Neurobiol Lipids Vol. 1, 7 (14 March 2003). Available at: http://neurobiologyoflipids.org/content/1/7/
Abstract: Cholesterol has recently received attention as a potentially important factor in Alzheimer's disease (AD) etiology. Caveolin, which binds cholesterol, plays a prominent role in cellular cholesterol transport. Here, we found a higher level of cholesterol and caveolin in the caveolae-enriched fractions prepared from AD patients' fibroblasts compared with age and sex matched controls (AC). Furthermore, the cross-linking activation of the prion protein, which is known to link to signal transduction of caveolin, is altered in AD fibroblasts. Our results suggest a dysregulation of cholesterol processing in AD fibroblasts which may contribute to the pathogenesis of AD.
Authors:Franck Dufour and colleagues
Authors Institution: Blanchette Rockefeller Neurosciences Institute, 9601 Medical Center Drive, Rockville, MD 20850, USA, fdufour[at]brni-jhu.org
Key words: Alzheimer's disease; amyloid beta precursor; APP; Down syndrome; etiology; lipids; lipoprotein; neurodegeneration marker; secretase; caveolin; caveolae; membrane; cell culture; human; non-neuronal tissue; neurodegenerative disease; signal transduction; prion; PKC; cross-linking; fractioning; biochemistry; triton
Abstract: Cholesterol has recently received attention as a potentially important factor in Alzheimer's disease (AD) etiology. Caveolin, which binds cholesterol, plays a prominent role in cellular cholesterol transport. Here, we found a higher level of cholesterol and caveolin in the caveolae-enriched fractions prepared from AD patients' fibroblasts compared with age and sex matched controls (AC). Furthermore, the cross-linking activation of the prion protein, which is known to link to signal transduction of caveolin, is altered in AD fibroblasts. Our results suggest a dysregulation of cholesterol processing in AD fibroblasts which may contribute to the pathogenesis of AD.
Authors:Franck Dufour and colleagues
Authors Institution: Blanchette Rockefeller Neurosciences Institute, 9601 Medical Center Drive, Rockville, MD 20850, USA, fdufour[at]brni-jhu.org
Key words: Alzheimer's disease; amyloid beta precursor; APP; Down syndrome; etiology; lipids; lipoprotein; neurodegeneration marker; secretase; caveolin; caveolae; membrane; cell culture; human; non-neuronal tissue; neurodegenerative disease; signal transduction; prion; PKC; cross-linking; fractioning; biochemistry; triton
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