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β‐Amyloid protein enhances the mitogen‐induced calcium response in circulating human lymphocytes
Author(s) -
Eckert Anne,
Hartmann Henrike,
Müller Walter E.
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80917-j
Subject(s) - neurotoxicity , calcium , amyloid (mycology) , stimulation , chemistry , mechanism of action , endocrinology , medicine , biology , in vitro , toxicity , biochemistry , inorganic chemistry
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 Ca 2+ 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 Ca 2+ 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.