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长期培养的神经元在衰老和神经学研究中的应用:铝神经毒性、突触退化与阿尔茨海默病

Application of long-term cultured neurons in aging and neurological research: aluminum neurotoxicity, synaptic degeneration and Alzheimer's disease.

作者信息

Kuroda Y, Kobayashi K, Ichikawa M, Kawahara M, Muramoto K

机构信息

Department of Molecular and Cellular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Japan.

出版信息

Gerontology. 1995;41 Suppl 1:2-6. doi: 10.1159/000213713.

DOI:10.1159/000213713
PMID:8537015
Abstract

Dissociated hippocampal and cerebral cortical neurons from rat embryonic brain form many synapses in culture. The neuronal networks in culture fire spontaneously in synchronous oscillation and can be maintained for long periods of up to 6 months. To establish the relevance of this long-term culture to aging and neurodegenerative diseases, effects of long-term exposure to aluminum, a risk factor for Alzheimer's disease, on the cultured cortical neurons were investigated. It appeared that aluminium promoted the aggregation of amyloid beta-protein and enhanced its neurotoxicity.

摘要

从大鼠胚胎脑中分离出的海马体和大脑皮层神经元在培养过程中形成了许多突触。培养中的神经元网络会自发地进行同步振荡放电,并且可以长时间维持,长达6个月。为了确定这种长期培养与衰老和神经退行性疾病的相关性,研究了长期暴露于铝(阿尔茨海默病的一个风险因素)对培养的皮层神经元的影响。结果表明,铝促进了β-淀粉样蛋白的聚集并增强了其神经毒性。

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Application of long-term cultured neurons in aging and neurological research: aluminum neurotoxicity, synaptic degeneration and Alzheimer's disease.长期培养的神经元在衰老和神经学研究中的应用:铝神经毒性、突触退化与阿尔茨海默病
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引用本文的文献

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p35/Cyclin-dependent kinase 5 is required for protection against beta-amyloid-induced cell death but not tau phosphorylation by ceramide.p35/细胞周期蛋白依赖性激酶5是抵御β-淀粉样蛋白诱导的细胞死亡所必需的,但对神经酰胺诱导的tau蛋白磷酸化并非必需。
J Mol Neurosci. 2007;31(1):23-35. doi: 10.1007/BF02686115.