Aluminum access to the brain: a role for transferrin and its receptor.
Aluminum access to the brain: a role for transferrin and its receptor.
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DOI：
10.1073/pnas.87.22.9024
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发表时间：
1990-11
影响因子：
11.1
通讯作者：
A. J. Roskams;J. Connor
中科院分区：
文献类型：
--
作者：
A. J. Roskams;J. Connor
铝在植物和动物细胞生物学中的毒性是公认的，尽管了解得很少。最近的几项研究已经确定铝是阿尔茨海默病、肌萎缩侧索硬化症和透析性痴呆的病理学中的一个潜在的（尽管存在很大争议）贡献因素。例如，在老年斑和神经纤维缠结中发现了高浓度的铝，这发生在患有阿尔茨海默病的受试者的大脑中。然而，铝（Al ~（3+））进入中枢神经系统（CNS）细胞的机制尚未被发现，在这里，我们描述了一个可能的途径，铝进入CNS细胞通过相同的高亲和力受体-配体系统，已被假定为铁（Fe ~（3+）传递到神经元和神经胶质细胞。这些结果表明，铝能够在正常生理条件下进入中枢神经系统。此外，这些数据表明，转铁蛋白和其受体之间的相互作用可能作为一个一般的金属离子调节系统在中枢神经系统中，扩展超出其假定的作用，在铁的调节。
The toxicity of aluminum in plant and animal cell biology is well established, although poorly understood. Several recent studies have identified aluminum as a potential, although highly controversial, contributory factor in the pathology of Alzheimer disease, amyotrophic lateral sclerosis, and dialysis dementia. For example, aluminum has been found in high concentrations in senile plaques and neurofibrillary tangles, which occur in the brains of subjects with Alzheimer disease. However, a mechanism for the entry of aluminum (Al3+) into the cells of the central nervous system (CNS) has yet to be found. Here we describe a possible route of entry for aluminum into the cells of the CNS via the same high-affinity receptor-ligand system that has been postulated for iron (Fe3+) delivery to neurons and glial cells. These results suggest that aluminum is able to gain access to the central nervous system under normal physiological conditions. Furthermore, these data suggest that the interaction between transferrin and its receptor may function as a general metal ion regulatory system in the CNS, extending beyond its postulated role in iron regulation.