摘要
背景:神经节苷脂在神经细胞膜上大量存在。神经节苷脂显示它与淀粉样蛋白 能相互作用,这种相互作用产生了阿尔兹海默病(AD)患者大脑淀粉样纤维的存在形式。一些早期的研究显示神经节苷脂新陈代谢的变化有助于AD的发病机制产生。方法:神经节苷脂从三个对照组中五个患有老年痴呆的病人大脑前庭中分离得到。神经节苷脂通过高效薄层色谱(HPTLC)检测,间苯二酚染色,免疫小鼠单克隆抗体的胆碱能神经元(神经节苷脂α哲-1)组化染色。结果。在所有的AD患者大脑中,不仅总的唾液酸含量,而且a系列神经节苷脂,GM1和GD1a,在与对照组相比急剧减少。这些结果是阿尔兹海默病发病机理的标志。相比之下,Chol-1α神经节苷脂GT1aα 和GQ1bα,是类胆碱(功)能的特异性标志物,在老年痴呆症患者的大脑中显著增加。结论:Chol-1α神经节苷脂的表达可能由类胆碱神经保护功能的修正所产生,并且在胆碱能突触传递中扮演了重要角色。
关键词: 阿尔兹海默病,Chol-1α抗原,胆碱能神经元,神经节苷脂,痴呆。
Current Alzheimer Research
Title:Brain Gangliosides in Alzheimer’s Disease: Increased Expression of Cholinergic Neuron-Specific Gangliosides
Volume: 14 Issue: 6
关键词: 阿尔兹海默病,Chol-1α抗原,胆碱能神经元,神经节苷脂,痴呆。
摘要: Background: Gangliosides are enriched in the neuronal membranes. Gangliosides are shown to interact with amyloid-β proteins, leading to formation of amyloid fibrils in Alzheimer’s disease (AD) brains. Several earlier studies indicated that the alterations of ganglioside metabolism could contribute the pathogenesis of AD.
Methods: Gangliosides were isolated from the frontal lobes in five patients with AD and three control subjects. Gangliosides were assessed by high performance thin-layer chromatography (HPTLC) with resorcinol staining and immunostaining using mouse monoclonal antibodies against cholinergic neuronspecific (Chol-1α) gangliosides. Results: In all AD brains, not only the total sialic acid content but also a-series gangliosides, GM1 and GD1a, were dramatically reduced as compared with those in control subjects. These results are a hallmark of the pathogenesis in AD. In contrast, Chol-1α gangliosides, GT1aα and GQ1bα, which are specific markers of cholinergic neurons, were significantly increased in AD brains. Conclusion: The expression of Chol-1α gangliosides may be caused by a compensation to preserve the function of the cholinergic neuron and play an important role in cholinergic synaptic transmission.Export Options
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Cite this article as:
Brain Gangliosides in Alzheimer’s Disease: Increased Expression of Cholinergic Neuron-Specific Gangliosides, Current Alzheimer Research 2017; 14 (6) . https://dx.doi.org/10.2174/1567205014666170117094038
DOI https://dx.doi.org/10.2174/1567205014666170117094038 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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