Bosman G J, Renkawek K, Van Workum F P, Bartholomeus I G, Marini S, De Grip W J
Department of Biochemistry, Faculty of Medicine, University of Nijmegen, The Netherlands.
J Neural Transm Suppl. 1998;54:248-57.
Anion exchange (AE) proteins are present in human neurons in the brain. Immunohistochemical data indicate that their apparent expression level increases with age, and especially with degeneration in Alzheimer's disease-affected brain areas. The increase in immunoreactivity is probably caused by changes in AE structure that lead to an increased accessibility of hitherto hidden epitopes. These epitopes correspond to regions in the membrane domain that are involved in generation of senescent cell-specific antigen from AE1 in aging erythrocytes. Elucidation of the molecular nature of these changes and the underlying mechanisms will lead to insight in the processes that govern aging- and degeneration-associated perturbation of membrane integrity. The functional consequences of changes in AE structure may range from acidosis and disturbance of cytoskeleton integrity to untimely or impaired recognition of neurons by microglia.
阴离子交换（AE）蛋白存在于人类大脑神经元中。免疫组织化学数据表明，它们的表观表达水平随年龄增长而增加，尤其是在阿尔茨海默病影响的脑区发生退化时。免疫反应性的增加可能是由AE结构的变化引起的，这种变化导致了迄今隐藏的表位更容易被识别。这些表位对应于膜结构域中与衰老红细胞中AE1产生衰老细胞特异性抗原有关的区域。阐明这些变化的分子本质及其潜在机制，将有助于深入了解控制衰老和退化相关的膜完整性扰动的过程。AE结构变化的功能后果可能从酸中毒和细胞骨架完整性紊乱到小胶质细胞对神经元的识别不及时或受损。
