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Thomas Jefferson University

2004

Farber Institute for Neuroscience Faculty Papers

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Similar Promotion Of Abeta1-42 Fibrillogenesis By Native Apolipoprotein E Epsilon3 And Epsilon4 Isoforms., David Sweeney, Ralph Martins, Harry Levine, Jonathan D Smith, Sam Gandy Aug 2004

Similar Promotion Of Abeta1-42 Fibrillogenesis By Native Apolipoprotein E Epsilon3 And Epsilon4 Isoforms., David Sweeney, Ralph Martins, Harry Levine, Jonathan D Smith, Sam Gandy

Farber Institute for Neuroscience Faculty Papers

The apolipoprotein E epsilon4 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 epsilon4 accumulate excess cerebral amyloid when compared to similarly prepared mice expressing human apolipoprotein E epsilon3. Therefore, it is important to search for relevant interactions(s) between apolipoprotein E epsilon4 and Abeta in order to clarify the biological role for apolipoprotein E epsilon4 in Alzheimer disease. Using a thioflavine T (ThT)-based assay, we have investigated the effects of native human apolipoprotein E isoforms on the kinetics of Abeta fibrillogenesis. No obvious …