Ibarreta D, Parrilla R, Ayuso M S
Department of Pathophysiology and Human Molecular Genetics, Centro de Investigaciones Biológicas (CSIC), Madrid, Spain.
Alzheimer Dis Assoc Disord. 1997 Dec;11(4):220-7.
The authors report calcium (Ca2+) homeostasis features of transformed lymphocytes from patients with late-onset Alzheimer disease and healthy age-matched controls. Alzheimer lymphoblasts show higher basal cytosolic-free [Ca2+] than controls. The antibodies anti-immunoglobulin M or the beta-amyloid (beta-amyloid) peptide fragment 25-35-induced elevation of cytosolic-free [Ca2+] was higher in Alzheimer disease lymphoblasts than in control cells. However, the kinetics of Ca2+ replenishment of Ca(2+)-depleted cells shows a higher accumulation of cytosolic Ca2+ in Alzheimer disease than in control lymphoblasts, which is better appreciated when the Ca2+ efflux is inhibited. Thus, the authors concluded that Alzheimer disease lymphoblasts have a lower Ca2+ buffering capacity than normal cells, probably because of changes in availability or intrinsic functional properties of the intracellular Ca(2+)-binding structures. Aging alters the kinetics of the Ca2+ replenishment in lymphoblasts in a manner that resembles Alzheimer disease. However, unlike Alzheimer disease, aging does not change the maximum cytosolic-free [Ca2+], suggesting that the mechanisms underlying the altered Ca2+ homeostasis in aging and late-onset Alzheimer disease are different.
作者报告了晚发性阿尔茨海默病患者和年龄匹配的健康对照者的转化淋巴细胞的钙（Ca2+）稳态特征。阿尔茨海默病淋巴细胞显示出比对照组更高的基础胞质游离[Ca2+]。抗免疫球蛋白M抗体或β-淀粉样蛋白（β-淀粉样蛋白）肽片段25-35诱导的胞质游离[Ca2+]升高在阿尔茨海默病淋巴细胞中比对照细胞更高。然而，Ca(2+)耗尽细胞的Ca2+补充动力学显示，阿尔茨海默病中胞质Ca2+的积累高于对照淋巴细胞，当Ca2+外流受到抑制时，这种差异更为明显。因此，作者得出结论，阿尔茨海默病淋巴细胞的Ca2+缓冲能力低于正常细胞，这可能是由于细胞内Ca(2+)结合结构的可用性或内在功能特性发生了变化。衰老以类似于阿尔茨海默病的方式改变了淋巴细胞中Ca2+补充的动力学。然而，与阿尔茨海默病不同的是，衰老不会改变最大胞质游离[Ca2+]，这表明衰老和晚发性阿尔茨海默病中Ca2+稳态改变的潜在机制是不同的。
