tailieunhanh - báo cáo hóa học: " β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: β-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins | Journal of Neuroinflammation BioMed Central Research Open Access p-Amyloid promotes accumulation of lipid peroxides by inhibiting CD36-mediated clearance of oxidized lipoproteins Vidya V Kunjathoor Anita A Tseng Lea A Medeiros Tayeba Khan and Kathryn J Moore Address Lipid Metabolism Unit Dept. of Medicine Massachusetts General Hospital Harvard Medical School Boston MA 02114 USA Email Vidya V Kunjathoor - kunjathoor@ AnitaA Tseng - tseng@ Lea A Medeiros - medeiros@ Tayeba Khan - Khan@ Kathryn J Moore - kmoore@ Corresponding author Published 16 November 2004 Received 08 October 2004 Accepted 16 November 2004 Journal of Neuroinflammation 2004 1 23 doi 1742-2094-1-23 This article is available from http content 1 1 23 2004 Kunjathoor et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Recent studies suggest that hypercholesterolemia an established risk factor for atherosclerosis is also a risk factor for Alzheimer s disease. The myeloid scavenger receptor CD36 binds oxidized lipoproteins that accumulate with hypercholesterolemia and mediates their clearance from the circulation and peripheral tissues. Recently we demonstrated that CD36 also binds fibrillar P-amyloid and initiates a signaling cascade that regulates microglial recruitment and activation. As increased lipoprotein oxidation and accumulation of lipid peroxidation products have been reported in Alzheimer s disease we investigated whether P-amyloid altered oxidized lipoprotein clearance via CD36. Methods The availability of mice genetically deficient in class A SRAI II and class B CD36 scavenger receptors