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Abnormal cholesterol processing in Alzheimer's disease patient's fibroblastsKeywords: 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.
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