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beta-Amyloid Protein Enhances the Mitogen-Induced Calcium Response in Circulating Human Lymphocytes

beta-Amyloid Protein Enhances the Mitogen-Induced Calcium Response in Circulating Human Lymphocytes

A Eckert, H Hartmann, W E Müller

FEBS Lett. 1993 Sep 6;330(1):49-52.

PMID: 8370457

Abstract:

The role of beta-amyloid in Alzheimer's disease and its cellular mechanism of action on neurons are still unclear. There is growing evidence that beta-amyloid or its fragment, 25-35, influence neuronal calcium regulation. To investigate the effects of beta-amyloid on calcium homeostasis in man we used peripheral human lymphocytes as a model system for central neurons. beta-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/l. 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 beta-amyloid's neurotoxicity. The lymphocyte seems to be a valuable model to study this effect in man.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4248092	Amyloid β 12-28 human			Price

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