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The amyloid β-peptide (Aβ) has a central role in initiating neurodegeneration in Alzheimer disease (AD) 1. It is widely believed to be an incidental catabolic byproduct of the amyloid β protein precursor (APP) with no normal physiological function.2

Aβ has been shown to be a ligand for a number of different receptors and other molecules3-5.  It is transported between tissues and across the blood brain barrierby complex trafficking pathways6.  Aβ is modulated in response to a variety of environmental stressors and is able to induce pro-inflammatory activities7.

Soluble amyloid β-peptide fragment that is a substrate for gelatinase A/type IV collagenase/MMP-2 and APP secretase; cleaved between Lys16 and Leu17.

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