Amyloid-beta (Abeta) has for a long time been thought to play a central role in the pathogenesis of Alzheimer disease (AD). Analysis of available data indicates that Abeta possesses properties of a metal-binding apolipoprotein influencing lipid transport and metabolism. Protection of lipoproteins from oxidation by transition metals, synaptic activity and role in the acute phase response represent plausible physiological functions of Abeta. However, these important biochemical qualities which may critically influence the development of AD, have been largely ignored by mainstream AD researchers, making Abeta appear to be a "black sheep" in a "good apolipoprotein" family. New studies are needed to shed further light on the physiological role of Abeta in lipid metabolism in the brain.