Eckert A, Förstl H, Hartmann H, Czech C, Mönning U, Beyreuther K, Müller W E
Department of Psychopharmacology, Central Institute of Mental Health, Mannheim, Germany.
Neuroreport. 1995 May 30;6(8):1199-202. doi: 10.1097/00001756-199505300-00031.
The amplifying effect of beta-amyloid fragment 25-35 (beta A25-35) on the mitogen-induced rise of free intracellular calcium in circulating lymphocytes was strongly reduced in 24 patients with Alzheimer's disease when compared with elderly, non-demented controls. Low beta-amyloid responses were significantly correlated with the presence of the apolipoprotein E epsilon 4 allele, suggesting a dose effect.
与老年非痴呆对照组相比,24例阿尔茨海默病患者中β-淀粉样蛋白片段25-35(βA25-35)对丝裂原诱导的循环淋巴细胞内游离钙升高的放大作用显著降低。低β-淀粉样蛋白反应与载脂蛋白Eε4等位基因的存在显著相关,提示存在剂量效应。