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The Interaction of Amyloid-β with ApoE

The form of beta amyloid is a partial determinant of the interaction with Apolipoprotein E

  • Chapter
Alzheimer’s Disease

Part of the book series: Subcellular Biochemistry ((SCBI,volume 38))

Abstract

Brain plaque deposition in the form of amyloid-beta (Aβ) peptide is a pathological hallmark of Alzheimer’s disease (AD). Apolipoprotein E (ApoE) is thought to be involved in plaque formation. Individuals afflicted with AD carrying the ApoE4 isoform have shown a greater number of Aβ plaques when compared to ApoE3 carriers, and inheritance of an ApoE4 allele increases the risk of AD when compared to ApoE2 and ApoE3 carriers. The role of ApoE in the pathogenesis of AD is not well understood but a hypothesis gaining widespread support is that ApoE is involved in deposition or clearance of Aβ by direct protein-to-protein interaction. We have established that various human Aβ conformations apparent during spontaneous aggregation confer differing degrees of binding to the three ApoE isoforms. When associated with lipid, ApoE4 bound preferentially to an intermediate aggregated form of Aβ and had higher avidity than did ApoE2 or ApoE3.

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  1. CNS Therapeutics, Pfizer Corporation, Kalamazoo, MI, USA

    Donald B. Carter

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  1. Donald B. Carter
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  1. Institute of Zoology, University of Mainz, Mainz, Germany

    J. Robin Harris

  2. Institute of Biochemistry, University of Mainz, Mainz, Germany

    Falk Fahrenholz

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Carter, D.B. (2005). The Interaction of Amyloid-β with ApoE. In: Harris, J.R., Fahrenholz, F. (eds) Alzheimer’s Disease. Subcellular Biochemistry, vol 38. Springer, Boston, MA . https://doi.org/10.1007/0-387-23226-5_13

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