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

FEBS Letters

Eckert, Anne¹  Müller, Walter E.¹  Hartmann, Henrike¹ 

[1] Central Institute of Mental Health, Department of Psychopharmacology, D-68159 Mannheim, Germany

关键词: β-Amyloid;    Human lymphocyte;    [Ca2+]i;    AD;    Alzheimer's disease;    βAPP;    β-amyloid precursor protein;    βA25-35;    β-amyloid fragment 25–35;    [Ca2+]i;    intracellular free calcium concentration;    EGTA;    ethylene glycol-bis (β-aminoethyl ether) N;    N;    N';    N'-tetraacetic acid;    PHA;    phytohemagglutinin;   

DOI  :  10.1016/0014-5793(93)80917-J

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown