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: Similar promotion of Aβ1-42 fibrillogenesis by native apolipoprotein E ε3 and ε4 isoforms | Journal of Neuroinflammation BioMed Central Research Open Access Similar promotion of Ap1-42 fibrillogenesis by native apolipoprotein E e3 and e4 isoforms David Sweeney1 Ralph Martins2 Harry LeVine III3 Jonathan D Smith4 and Sam Gandy 5 Address 1Cornell University Medical College 1300 York Ave Room A569 New York NY 10021 USA 2Sir James McCusker Alzheimer s Unit The University of Western Australia Perth WA Australia 6009 3Sanders-Brown Institute on Aging University of Kentucky Lexington KY 40508 USA 4Cleveland Clinic Cleveland OH 44195 USA and 5Farber Institute for Neurosciences Thomas Jefferson University 900 Walnut Street JHN 467 Philadelphia PA 19107-5587 USA Email David Sweeney - sweeney@ Ralph Martins - rmartins@ Harry LeVine - hlevine@ Jonathan D Smith - smithj@ Sam Gandy - samgandy3d@ Corresponding author Published 16 August 2004 Received 07 August 2004 Journal of Neuroinflammation 2004 1 15 doi l742-2094-l-l5 Accepted 16 August 2004 This article is available from http content l l l5 2004 Sweeney 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 The apolipoprotein E e4 allele contributes to the genetic susceptibility underlying a large proportion 40-60 of typical sporadic Alzheimer disease. Apolipoprotein E deficient mice made transgenic for human apolipoprotein E e4 accumulate excess cerebral amyloid when compared to similarly prepared mice expressing human apolipoprotein E e3. Therefore it is important to search for relevant interactions s between apolipoprotein E e4 and Ap in order to clarify the biological role for apolipoprotein E e4 in Alzheimer disease. Using a thioflavine T ThT -based assay we have .
