Bosman G J, Bartholomeus I G, de Man A J, van Kalmthout P J, de Grip W J
Department of Biochemistry, University of Nijmegen, The Netherlands.
Neurobiol Aging. 1991 Jan-Feb;12(1):13-8. doi: 10.1016/0197-4580(91)90033-g.
Erythrocytes from patients with Alzheimer's disease show signs of disturbance of the normal cellular aging process. Immunoblotting of erythrocyte membrane proteins from Alzheimer patients reveals increased breakdown of the anion transport protein band 3 in a majority of the cells, similar to what is observed in only a very small cell population during normal aging. These structural changes are accompanied by changes in anion transport characteristics, but the latter partially deviate from those observed during normal aging. The amount of erythrocyte-bound immunoglobulin G, the most direct and relevant parameter of erythrocyte aging, is significantly increased in Alzheimer patients relative to age-matched, healthy donors and to patients with multi-infarct dementia. These data indicate accelerated molecular breakdown of band 3 and premature appearance of senescent cell characteristics in erythrocytes from Alzheimer patients, and support the hypothesis that abnormal cellular aging may be involved in the etiology of the Alzheimer-specific pathology.
阿尔茨海默病患者的红细胞显示出正常细胞衰老过程受到干扰的迹象。对阿尔茨海默病患者红细胞膜蛋白进行免疫印迹分析发现，大多数细胞中阴离子转运蛋白带3的降解增加，这与正常衰老过程中仅在非常小的细胞群体中观察到的情况相似。这些结构变化伴随着阴离子转运特性的改变，但后者部分偏离了正常衰老过程中观察到的情况。相对于年龄匹配的健康供体和多发性梗死性痴呆患者，阿尔茨海默病患者红细胞结合免疫球蛋白G的量（红细胞衰老最直接且相关的参数）显著增加。这些数据表明，阿尔茨海默病患者红细胞中带3的分子降解加速，衰老细胞特征过早出现，并支持异常细胞衰老可能参与阿尔茨海默病特异性病理病因学的假说。
