β‐Amyloid protein enhances the mitogen‐induced calcium response in circulating human lymphocytes

Abstract

The role of β-amyloid in Alzheimer's disease and its cellular mechanism of action on neurons are still unclear. There is growing evidence that β-amyloid or its fragment, 25–35, influence neuronal calcium regulation. To investigate the effects of β-amyloid on calcium homeostasis in man we used peripheral human lymphocytes as a model system for central neurons. β-Amyloid fragment 25–35 exposed to lymphocytes for 60 s elevates the phytohemagglutinin (PHA)-induced Ca²⁺ rise in a dose-dependent manner. Small effects were already seen at concentrations as low as 50 nmol/1. Similar effects were also observed with fragment 1–40, whereas fragments 1–28 or 12–28 did not affect the Ca²⁺ response after PHA stimulation. Our findings support the hypothesis of an enhanced calcium response as a general feature of β-amyloid's neurotoxicity. The lymphocyte seems to be a valuable model to study this effect in man.