Rui Yanfang, Li Ruxin, Liu Yifu, Zhu Shaoqing, Yu Xinzhu, Sheng Zhonghua, Xie Zuoping
Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing 100084, China.
Cell Biol Int. 2006 Sep;30(9):733-40. doi: 10.1016/j.cellbi.2006.05.005. Epub 2006 May 16.
The effects of beta amyloid (Abeta) on cytoplasmic Ca(2+) (Ca(2+)) have been studied extensively, but the current literature on this aspect is confusing. We reported that 20 microM Abeta(25-35) significantly inhibited the synchronized spontaneous cytoplasmic Ca(2+) transients immediately after application, whereas it had little effect on the baseline Ca(2+) concentration in neurons. Abeta(1-42) had a similar effect on the Ca(2+) transients as Abeta(25-35), while it increased baseline Ca(2+) concentration gradually. However, Abeta(1-40) had little effect on either Ca(2+) transients or baseline Ca(2+). Such differential effects of Abeta on Ca(2+) signals might explain, at least partially, the confusing observations from the previous studies and provide important therapeutic implications for preventing or reversing early neuron damage in Alzheimer's disease.
