A behavioral and ultrastructural dissection of the interference of aluminum with aging.
A behavioral and ultrastructural dissection of the interference of aluminum with aging.
复制标题
铝对衰老干扰的行为和超微结构剖析。
DOI：
10.3233/jad-2004-6312
复制
发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Mircea Miclea
中科院分区：
文献类型：
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作者：
A. Miu;A. Olteanu;Mircea Miclea
神经科学家一直在探索铝（Al）对阿尔茨海默病（AD）发病机制的可能贡献，导致大量研究详细说明了这种金属的生物毒性。然而，到目前为止，已经有一些帐户的干扰铝与衰老及其相关性的发病机制的AD。我们研究了青年和老年大鼠暴露于葡萄糖酸铝三个月的行为和海马中铝的超微结构特征。老年动物表现出活动和情绪性评分下降，铝暴露的老年男性改变了情绪反应行为。电镜分析表明，铝可促进衰老海马细胞和超微结构的退行性改变，如颗粒空泡变性、脂褐素和淀粉样蛋白在神经元和星形胶质细胞胞浆及细胞外区室沉积、Hirano小体、脱髓鞘和线粒体萎缩等。此外，对随机选择的样品测量的髓鞘宽度和线粒体直径的定量证实了髓鞘和线粒体是Al毒性的主要靶标。脱髓鞘和线粒体萎缩似乎更先进的铝暴露的老年男性的海马，支持的行为结果所建议的性别的影响。这些发现和其他附带的结果也报告在这里讨论的背景下，可能参与的铝在AD，介导的老化和催化的肝脏形态病理学。
The persistence of neuroscientists in exploring aluminium's (Al) possible contribution to the pathogenesis of Alzheimer's disease (AD) has resulted in a wealth of researches detailing the biological toxicity of this metal. However, to date, there have been few accounts of the interference of Al with aging and its relevance to the pathogenesis of AD. We investigated the behavioral and the ultrastructural signatures of Al in the hippocampus on young and aging rats which were exposed for three months to aluminium gluconate. The aging animals displayed decreased scores of activity and emotionality, and the Al-exposed aging males had altered emotional reactivity behaviors. The electron-microscopic analysis indicated that Al promoted in the aging hippocampus a variety of cellular and ultrastructural degenerative signs, such as granulo-vacuolar degenerations, deposition of lipofuscin and amyloid in the cytoplasm of neurons and astrocytes, and in extracellular compartments, Hirano bodies, demyelination and the atrophy of the mitochondria. Moreover, the quantitation of myelin sheath width and the diameter of mitochondria measured on randomly selected samples confirmed that myelin and mitochondria are primary targets of Al's toxicity. Demyelination and mitochondrial atrophy seemed more advanced in the hippocampus of Al-exposed aging males, supporting the effect of sex suggested by the behavioral results. These findings and other collateral results also reported here are discussed in the context of a possible involvement of Al in AD, mediated by aging and catalyzed by hepatic morphopathology.