Abstract

The Alzheimer amyloid peptides are the main constituent of the diagnostic hallmark of Alzheimer disease, the senile plaque. A halo of neurodegeneration surrounds the senile plaques observed in the brains of Alzheimer patients. Significant efforts are under way to determine whether the Alzheimer peptides are the causal agents of this neurodegeneration. We review the developments in identifying the putative interaction sites of Alzheimer amyloid peptides on cells and intact brain tissue. We focus on the specificity of this interaction and on the molecular nature of potential receptors. These studies form the bases for developing therapeutics that target potential interaction sites and inhibit Alzheimer amyloid peptide deposition.

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