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Abnormal cholesterol processing in Alzheimer's disease patient's fibroblasts

Author(s): Franck Dufour | Wei-Qin Zhao | Lakshmi Ravindranath | Daniel L. Alkon

Journal: Neurobiology of Lipids
ISSN 1683-5506

Volume: 1;
Start page: 34;
Date: 2003;
Original page

Keywords: 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

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.
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